Four major causes of vision loss in the older adult

 direct and indirect costs of the four major causes of vision loss in the older adult are between $30 billion and $40 billion each year 

Poor tolerance of glare is also a problem for many older adults as they age. 

EYE_ Jargon

FDT
Flicker
glaucoma
HPRP
Matrixmotion perimetry
perimetryprogression
Pulsar
Rarebit
SAP
SWAP
visual fields
 For AMD -5 Preferential Hyperacuity Perimeter (PHP) -5
Foresee PHP (Notal Vision)
For Retina Micro Perimeter MP-I (Nidek)
• Advanced biometry Partial Coherence Laser Interferometer
Non-contact Optical Coherence Biometry
Laser Interferometry Technique
• Advanced High Definition AB-Scan IJSG
Aviso (Quantel Medical)
VuMax II (Sonomed)
• Standard diaital fundus camera with FFA
 Advanced anterior examination
— Pachy-Autorefrakto-Keratometer
• PARK 1 (OCULUS Optikgeräte GmbH)
• Galilei G4 (Ziemer) -5 Placido and Dual Scheimpflug
— Anterior Optical Coherence Tomography
• Visante OCT (Carl Zeiss Meditec AG)
• SL OCT (Heidelberg Engineering)

— Anterior Optical Coherence Tomography 

• Visante OCT (Carl Zeiss Meditec AG) 

• SL OCT (Heidelberg Engineering) 

• TOMEY SS-1000 (TOMEY GmbH) 

Scheimpflug Camera Pentacam Keratometry, Corneal 

topography, Pachimetry, Corneal wavefront, AC and angle 

analyzer, Lens analyzer, Phakic IOL and Post refractive surgery 

biometry 

• Pentacam HR (OCULUS Optikgeräte GmbH) 

• Advanced anterior examination 

— Keratograph Oculus Keratograph (OCULUS 

Optikgeräte GmbH) 

— Endothelium Specular Microscope 

— Advanced High Definition Ultrasound Biomicroscopy 

(UBM) 

• P60 UltrasoudBioMicroscope (Paradigm) 

• Aviso (Quantel Medical) 

• VuMax (Sonomed) 

— Very high frequency (VHF) ultrasound eye scanner 

Advanced posterior examination 

— Posterior Optical Coherence Tomography 

• Stratus OCT (Carl Zeiss Meditec AG) 

• 3D OCT 2000 FA Plus Swept-Source SS OCT and 

DRI (Topcon) 

• 3D OCT-I Maestro OCT (Topcon) 

• RS3000 Advance (Nidek) 

• RTVue FD OCT (Optovue) 

• High Definition Cirrus + SmartCube HD OCT (Carl 

Zeiss Meditec AG) 

• SOCT Copernicus (Reichert) 

• HRA OCT Spectralis (Heidelberg Engineering) 

• Envisu Pediatric SDOCT (bioptigen) 

Addison’s disease

Addison’s disease Overview Definition Addison’s disease occurs when the adrenal glands do not produce enough cortisol and, in some cases, aldosterone. There are two types of adrenal insufficiency: primary and secondary. Primary adrenal insufficiency (Addison’s disease) is caused by adrenal gland malfunction. Secondary adrenal insufficiency is much more common than primary adrenal insufficiency and is due to pituitary malfunction and a lack of adrenocorticotrophic hormone (ACTH)1 CPPC c01.tex V2 - 11/18/2015 1:44 P.M. Page 8 ❦ ❦ ❦ ❦ 8 Addison’s disease A Risk factors Addison’s disease has a prevalence of 93–140 per million people and annual incidence of 4.7–6.2 per million people in western populations Differential diagnosis The onset of Addison’s disease is often insidious. Its usual symptoms (such as fatigue, lethargy, weakness and low mood) are non-specific and highly prevalent in the general population, and overlap with many other common conditions, including: ● depression ● chronic fatigue syndrome ● anorexia nervosa ● type 1 diabetes ● gastrointestinal disorders Diagnostic tests About half of patients with Addison’s disease are diagnosed only after an acute adrenal crisis. A diagnosis of Addison’s disease is made by laboratory tests, firstly to determine whether levels of cortisol are insufficient and then to establish the cause. A short Synacthen test is the investigation of choice to confirm or exclude Addison’s disease. 250 micrograms of tetracosactide (an analogue of corticotropin) is administered by intramuscular or intravenous injection and three blood samples for serum cortisol are taken immediately, at 30 minutes and at 60 minutes. A normal response is a rise in serum cortisol level to above 500 nmol/L at 30 minutes or 60 minutes. A level less than 100 nmol/L indicates a high likelihood of adrenal insufficiency. A plasma ACTH concentration should be measured, as a raised concentration will distinguish Addison’s disease from secondary adrenal insufficiency. Once the diagnosis of Addison’s disease is made, further investigations are needed to determine the underlying cause Treatment goals Replacing or substituting the adrenal hormones Treatment options ● Hydrocortisone ● Prednisolone ● Fludrocortisone Pharmaceutical care and counselling1,2 Essential intervention Cortisol is replaced orally with hydrocortisone tablets, usually given once or twice daily. If aldosterone is also deficient, it is replaced with oral doses of fludrocortisone acetate taken once a day. Patients receiving aldosterone replacement therapy are usually advised to increase their salt intake. The doses of each of these medications are adjusted to meet the needs of individual patients Essential intervention The usual replacement dose of hydrocortisone is 15–25 mg/day, given in two or three divided doses. Fludrocortisone is given in a single dose of 50–200 micrograms a day. Doses do not have to be matched to meals so patients can take to suit their lifestyle Secondary intervention Medication may need to be increased (doubled or tripled) during times of stress, infection or injury. This should be given parenterally if a patient cannot tolerate the drug orally. A patient with an acute adrenal crisis needs urgent hospital admission for intravenous fluid, parenteral hydrocortisone and treatment of the precipitating cause CPPC c01.tex V2 - 11/18/2015 1:44 P.M. Page 9 ❦ ❦ ❦ ❦ Adrenaline: nebulised 9 Continued A monitoring There are no objective measures for assessing the effectiveness of treatment. Monitor for signs of: ● Overreplacement: hypertension, thin skin, striae, easy bruising, glucose intolerance, hyperglycaemia, electrolyte abnormalities ● Underreplacement: symptoms of Addison’s disease, including fatigue, postural hypotension, nausea, weight loss and salt craving

CCH_Acute kidney injury

Acute kidney injury Overview Definition Clinically acute kidney injury (AKI) is characterised by a rapid reduction in kidney function over hours or days, resulting in a failure to maintain fluid, electrolyte and acid–base homeostasis. Untreated this can lead to pulmonary oedema, hyperkalaemia and metabolic acidosis. AKI is defined when one of the following criteria is met.
● Increase in serum creatinine of ≥26 micromol/L within 48 hours
● Increase in serum creatinine of ≥50% from baseline (the lowest serum creatinine value recorded within 3 months of the event), which is known or presumed to have occurred within the past 7 days
 ● Fall in urine output to <0 .5="" for="" hour="" kg="" ml="">6 consecutive hours in adults and >8 hours in children Causes Prerenal AKI ( ≈80% of cases) Blood flow to the kidney is reduced which, if left untreated, can lead to ischaemic injury to the kidney (known as acute tubular necrosis or ATN). Common causes of prerenal AKI include: 
● hypotension
● dehydration
● sepsis
● significant blood loss, e.g. gastrointestinal bleeding
● cardiac or liver failure
● severe burns Some medications may cause prerenal AKI, such as NSAIDs, ACE inhibitors, ARBs and diuretics (see ‘Further reading’ for more detailed information). Postrenal AKI ( ≈10% of cases) Obstruction to urine outflow from the kidneys occurs. Common causes of postrenal AKI include: ● benign prostatic hypertrophy
● bladder or prostate cancer
● abdominal tumours compressing the urinary tract
● renal stones Some medications may cause postrenal AKI, either through deposition of crystals (e.g. aciclovir or cytotoxic agents) or through blood clots after bleeding (e.g. antiplatelet or anticoagulant therapy) CPPC c01.tex V2 - 11/18/2015 1:44 P.M.

 Acute kidney injury
 Intrinsic AKI ( ≈10% of cases) A Damage occurs to the kidney itself, often immunological in origin. Common causes of intrinsic AKI include:
● acute interstitial nephritis (AIN) – a hypersensitivity reaction that may often be drug-related, e.g. proton pump inhibitors (PPIs) and pencillins
● myeloma – through deposition of light chains in the kidney
● autoimmune renal disease, including lupus and vasculitis
● rhabdomyolysis – due to the renal toxicity of myoglobin from muscle breakdown Risk factors
● Age >75 years
● Chronic kidney disease
● Cardiac failure
● Peripheral vascular disease
● Liver disease
● Diabetes mellitus
● Nephrotoxic medications, including iodinated radiological contrast media
● Hypovolaemia
● Sepsis
● Surgical procedures Diagnostic tests
● Drug history
● Vital signs (temperature, heart rate, blood pressure)
● Biochemistry (urea and electrolytes)
● Full blood count
 Urine dipstick ± microscopy
● Microbiology:
● Urine culture
● Blood culture
● Urine output
● Hydration status, including jugular venous pressure More specific renal investigations are dependent upon the clinical presentation and may include:
● renal immunology
● urinary biochemistry (electrolytes, osmolality)
● renal tract ultrasound within 24 hours (if renal tract obstruction is suspected)
● kidney biopsy Staging The severity of AKI can be classified into three stages. 2 Stage 1: serum creatinine increase of ≥26 micromol/L within 48 hours or increase to ≥1.5–1.9 times baseline; urine output <0 .5="" for="" hour="" kg="" ml="">6 consecutive hours Stage 2: serum creatinine increased to ≥2–2.9 times baseline; urine output <0 .5="" for="" hour="" kg="" ml="">12 hours Stage 3: serum creatinine increased to ≥3 times baseline or increased to ≥354 micromol/L or commenced on renal replacement therapy, irrespective of stage; urine output <0 .3="" for="" hour="" kg="" ml="">24 hours or anuria for 12 hours CPPC c01.tex V2 - 11/18/2015 1:44 P.M.

 Acute kidney injury A Treatment goals AKI has a poor prognosis, with the mortality ranging from 10% to 80%. depending upon the patient population studied. Even small increases in serum creatinine are associated with worse patient outcomes, including prolonged hospital stay and increased morbidity and mortality. 3 The goals of AKI treatment are:
● Prevention
● Early identification and assessment
● Appropriate hydration
● Avoid hypotension (systolic blood pressure
<110 mmhg="" nbsp="" p="">● Prompt treatment of infection and other medical conditions
● Stop nephrotoxic drugs
● Adjust doses of renally excreted drugs Treatment options
● Identify and treat potential causes, e.g. underlying sepsis
● Assess volume status and give appropriate intravenous fluid therapy
● Use potassium-containing solutions (e.g. Hartmann’s) cautiously due to the risk of exacerbating hyperkalaemia
● Daily observations, fluid balance, body weight and urine output should be monitored to ensure appropriate fluid therapy and avoid overload
● Medication review:
● Discontinue/avoid all nephrotoxic medications
● Discontinue antihypertensive medications if patient is hypotensive
● Adjust medication doses as necessary
● Administer vasopressors and/or inotropes to increase blood pressure where appropriate
● Manage biochemical complications, e.g. treatment of hyperkalaemia and/or metabolic acidosis
● Give renal replacement therapy Pharmaceutical care and counselling Assess
● Ensure a detailed drug history is taken, including OTC, herbal and recently stopped medications
● Fluid status
● Medication review Essential intervention Many drugs can precipitate AKI and all nephrotoxic medications or medications that may affect renal haemodynamics should be stopped or avoided, e.g. NSAIDs, ACE inhibitors and diuretics. Advise on suitable alternatives where appropriate Essential intervention Review the side-effect profile of all medicines to identify potential causes of ATN or interstitial nephritis, e.g. amphotericin, PPIs Essential intervention Discontinue non-essential medications where appropriate until AKI has resolved, e.g. statins Essential intervention Advise on appropriate drug dosing in AKI. Many pharmacokinetic parameters, including volume of distribution, clearance and protein binding, are altered in AKI. Drug doses need to be adjusted appropriately with the correct assessment of kidney function to reduce toxicity. Examples include dose reduction of renally excreted drugs such as digoxin or gabapentin, or use of alternative agents that are less renally excreted, e.g. switching from morphine to fentanyl CPPC c01.tex V2 - 11/18/2015 1:44 P.M.


Secondary
A intervention Advise on the appropriate use of intravenous fluids (see Fluid balance entry). Provide recommendations around fluid restriction and minimum infusion volumes for drugs used in fluid-overloaded patients Continued monitoring Daily assessment of renal function and review of medication doses as renal function improves. Consider reintroduction of non-causative medications once AKI has resolved Counselling Counsel a patient regarding any medication changes prior to discharge, in particular any causative agents that have now been stopped. Advise patients about any medications to be avoided in future (e.g. OTC NSAIDs). Advise patients receiving medications that put them at risk of AKI to seek medical advice if they become acutely unwell or think they might be dehydrated. Provide accurate discharge information to general practitioners, including changes to medication, medicines to be restarted after discharge (and when this should occur) and any counselling provided/

CCH_Acetylcysteine for nebulisation

Acetylcysteine for nebulisation 

Acetylcysteine injection is sometimes used in an unlicensed capacity as a mucolytic.
1 The adult dose is 3 –5 mL of acetylcysteine 20% injection, or 6 –10 mL of a 10% solution through a face mask or mouthpiece, nebulised three or four times daily with air (use of concentrated oxygen causes degradation). Acetylcysteine reacts with some materials, e.g. rubber, iron, copper and nickel, so ensure the nebuliser does not contain these. Nebulisation equipment should be cleaned immediately after use with hot water and left to air dry. Acetylcysteine may induce bronchospasm. As a precaution this can be avoided by either administration of a lower dose, diluting 1 mL of CPPC c01.tex V2 - 11/18/2015 1:44 P.M. 
A acetylcysteine 20% injection in 5 mL sodium chloride 0.9% and nebulising 3 –4 mL, or preadministering a nebulised bronchodilator. Alternatively 1 –10 mL of a 20% solution or 2 –20 mL of a 10% solution may be given by nebulisation every 2 –6 hours.

CCH_ACE inhibitor-induced cough

ACE inhibitor-induced cough

Chronic cough is a well-described class effect of angiotensin converting enzyme (ACE) inhibitors.

The cough is typically dry and is associated with a tickling or scratching sensation in the throat. Reports vary; 5 –35% of patients who receive ACE inhibitors develop a dry cough, sometimes severe enough to require discontinuation of the drug.

ACE inhibitor cough is considered a class effect that may occur with any ACE inhibitors and is not dose-dependent. Cough may occur within hours of the first dose of medication, or its onset can be delayed for weeks to months after the initiation of therapy.
Treatment with ACE inhibitors may sensitise the cough reflex, thereby potentiating other causes of chronic cough. 3 Although cough usually resolves within 1 –4 weeks of cessation of therapy with the offending drug, in a subgroup of individuals cough may linger for up to 3 months. Women and those of black or Asian ethnicity have been reported to be at increased risk of ACE inhibitor cough. Mechanisms of cough from ACE inhibitors The inhibition of ACE prevents the conversion of angiotensin I to angiotensin II, with consequent salutary benefits via the renin– angiotensin system in pathological states. ACE inhibitor cough is thought to be linked to the suppression of ACE, which is proposed to result in an accumulation of substances normally metabolised by ACE: bradykinin and substance P. However, the development of cough may result from a more complex cascade of events than originally believed. Bradykinin has been shown to induce the production of arachidonic acid metabolites and nitric oxide, and there is some evidence that these products, which are subject to regulation by other pathways, may promote cough through proinflammatory mechanisms.

Can angiotensin II receptor blockers be used in patients with a history of ACE inhibitor cough?

Theoretically, angiotensin II receptor blockers (ARBs) should not induce cough as they do not directly inhibit ACE activity or inhibit the breakdown of bradykinin. Indeed, ARBs have been associated with a low incidence of cough in patients with a history of ACE inhibitor cough, e.g. the frequency of cough with losartan was lower than with lisinopril (29 versus 72%, P < 0.01), and similar to hydrochlorothiazide (34%). 5 CPPC c01.tex V2 - 11/18/2015 1:44 P.M.

 A Treatment of ACE inhibitor cough 

The only uniformly effective intervention for ACE inhibitor-induced cough is the cessation of therapy with the offending agent. In cases in which the continuation of an ACE inhibitor is necessary despite cough, cromoglicate, baclofen, theophylline and local anaesthetics have been reported to be of some benefit, although none has been subjected to large-scale trials.

 Since the use of ACE inhibitors is now widespread, it is vitally important that practitioners consider identifying cases of ACE inhibitor-induced cough.
Available studies indicate that, in the great majority of patients, those who develop these adverse reactions from ACE inhibitors can tolerate ARBs. The cardiovascular benefits and potential reduction in mortality from use of these drug classes are important and significant.

 Therefore, in a risk–benefit assessment, consideration should be given to the cautious alternative use of ARBs in the management of patients who develop cough from ACE inhibitors.

ABCD2 scoring system TIA and stroke risk

ABCD2 scoring system

 The ABCD2 score is a validated risk assessment tool designed to identify individuals at high early risk of subsequent stroke after a transient ischaemic attack (TIA). Assessing people rapidly can minimise the chances of a full stroke occurring, as there is a 20% risk of a full stroke within the first 4 weeks after a TIA.
1,2 SCORING SYSTEM
Clinical feature Score A – Age (≥60 years) 1 B – Blood pressure at presentation (≥140/90 mmHg) 1 C – Clinical features: unilateral weakness 2 speech disturbance without weakness 1 D – Duration of symptoms: ≥60 minutes 2 10–59 minutes 1 D – Diabetes mellitus 1 Total ABCD2 score 0–7 Interpretation3,4 Early risk of stroke after TIA: 2-day risk of stroke: Scores 0–3: low risk, 1% Scores 4–5: moderate risk, 4.1% Scores 6–7: high risk, 8.1%
● People with a score of ≥4 are regarded as being at a higher risk of early stroke. Aspirin 300 mg daily should be started immediately and specialist assessment (exclusion of stroke mimics, identification of vascular treatment, identification of likely causes) and investigation should happen (in a TIA clinic) within 24 hours of onset of symptoms.
 ● People with a score of ≤3 are considered at lower risk but should also start aspirin 300 mg daily and have specialist assessment and investigation within a maximum of 7 days of onset of symptoms

Prescription jargon

DOSES
od /qDonce daily
bd/BID twice daily
tds /TID three times daily
qds/QID four times daily

ROUTES
im intramuscular
inh inhaled
iv intravenous
ivi intravenous infusion
neb via nebuliser
nocte  at night
mane in the morning
prn as required
stat at once
po oral
pr  per rectal
sc subcutaneous
top topical
sl sublingual

5-ASA
SHT
ASCE
AAC
Ab
abdo
ABPM
ACC
ACCP
ACh
ACS
ADP
Ag
AHA
AKI
ALP
ALS
5-aminosalicylic acid
5-hydroxytryptamine (z serotonin)
accident and emergency
antibiotic-associated colitis
antibody
abdomen/abdominal
ambulatory blood pressure monitoring
American College of Cardiology
American College of Chest Physicians
ACE inhibitor
acetylcholine
acute coronary syndrome
adenosine phosphate
atrial fibrillation
antigen
American Heart Association
acute kidney injury
acute lymphoblastic leukaemia
alkaline phosphatase
adult life support (algorithms of European
ALS
ALT
AMTS
ANA
ARB(s)
ARDS
AS
ASAP
assoc
AST
AV
AVM
adult life support (algorithms of European
Resuscitation Council)
alanine(-amino) transferase
acute myocardial infarction
abbreviated mental test score (same as MT S)
anti-nuclear antigens
activate partial thromboplastin time
angiotensin receptor blocker(s)
adult respiratory distress syndrome
aortic stenosis
as soon as possible
associated
aspartate transammase
arteriovenous
arteriovenous malformation
AVN
AZT
BBB
BCSH
BCT
BHS
BIH
BIPAP
BM
BMI
BPH
BTS
c
atrioventricular node
zidovudine
bundle branch block
British Committee for Standards in Haematology
broad complex tachycardia
blood flow
serum blood glucose in mmol/l; see also CBG
British Hypertension Society
benign intracranial hypertension
bilevel/biphasic positive airway pressure
bone marrow (NB: BM is often used, confusingly,
to signify finger-prick glucose; CBG (capillary blood
glucose) is used for this purpose in this book)
body mass index = weight (kg)/height (m)2
blood pressure
benign prostatic hypertrophy
British Thoracic Society
biopsy
constlpatlon
cancer (NB: calcium is abbreviated to Ca2+)
BTS
c
Ca
CAH
CBF
CBG
CCF
CCU
cf
CK
CKD
CLL
CML
CMV
CNS
British Thoracic Society
biopsy
constlpatlon
cancer (NB: calcium is abbreviated to Ca2+)
congenital adrenal hyperplasia
cerebral blood flow
capillary blood glucose in mmol/l (finger-prick testing)
(NB: BM is often used to denote this, but this is
confusing and less accurate and thus not used in
this book)
congestive cardiac failure
Coronary Care Unit
compared with
contraindicated
creatine kinase
chronic kidney disease
chronic lymphocytic leukaemia
chronic myelogenous leukaemia
cytomegalovirus
central nervous system

co
COPD
cox
CPR
CRF
CRP
CSF
CSM
CT
CVA
CVP
CXR
DA
DCT
dfx
cardiac output
chronic obstructive pulmonary disease
cyclo-oxygenase
cardiopulmonary resuscitation
chronic renal failure
C reactive protein
cerebrospinal fluid
Committee on Safety of Medicines
computerised tomography
cerebrovascular accident
central venous pressure
chest X-ray
diarrhoea
dopamine receptor subtype1/2/3
diarrhoea and vomiting
dopamine
distal convoluted tubule
defects
diabetes insipidus
DIC
DIGAMI
DKA
DMARD
dt
DWI
e'lyte
EBV
ECG
ECT
ENT
disseminated intravascular coagulation
glucose, insulin and potassium intravenous infusion
used in acute myocardial infarction
diabetic ketoacidosis
diabetes mellitus
disease-modifying anti-rheumatoid arthritis drug
due to
diffusion weighted (imaging); specialist MRI mostly
used for strokeÆIA
diagnosis
eosinophils
electrolyte
Epstein—Barr virus
electrocardiogram
electroconvulsive therapy
ejection fraction
ear, nose and throat
EPSE
ERC
ESC
ESR
exac
FBC
FFP
FHx
Fi02
FMF
fx
G6PD
GABA
GBS
GCS
GFR
GI
GIK
extrapyramidal side effects
European Resuscitation Council
European Society of Cardiology
erythrocyte sedimentation rate
exacerbates
full blood count
iron
fresh frozen plasma
family history
inspired 02 concentration
familial Mediterranean fever
effects
glucose-6-phosphate dehydrogenase
gamma aminobutyric acid
Guillain—Barré syndrome
Glasgow Coma Scale
glomerular filtration rate
gastrointestinal
glucose, insulin and K + infusion
GFR
GI
GIK
GMC
GTN
GU
HBPM
Hct
HDL
HIV
FILA
HMG-CoA
HONK
hrly
glomerular filtration rate
gastrointestinal
glucose, insulin and K + infusion
General Medical Council (of UK)
glyceryl trinitrate
genitourinary
hour(s)
hypertrophic (obstructive) cardiomyopathy
haemoglobin
heart block
home blood pressure monitoring
haematocrit
high-density lipoprotein
heart failure
human immunodeficiency virus
human leucocyte antigen
3-hydroxy-3-methyl-glutaryl coenzyme A
hyperosmolar non-ketotic state
hourly
HSV
HTN
HUS
IBD
IBS
IBW
ICP
ICU
IHD
IL-2
Inc
inh
INR
IOP
herpes simplex virus
height
hypertension
haemolytic uraemic syndrome
history
inflammatory bowel disease
irritable bowel syndrome
ideal body weight (see p. 268 for details)
intracranial pressure
intensrve care unit
ischaemic heart disease
interleukin-2
intramuscular
including
inhaled
international normalised ratio (prothrombin ratio)
intraocular pressure
immune/idiopathic thrombocytopenic purpura
intensive therapy unit
intravenous
iv
IVDU
ivi
Ix
LA
LBBB
LDL
LF
LFTs
LMWH
LVF
mane
immune/idiopathic thrombocytopenic purpura
intensive therapy unit
intravenous
intravenous drug user
intravenous infusion
Investigation
potassium (serum levels unless stated otherwise)
lymphocytes
long-acting
left bundle branch block
low-density lipoprotein
liver failure
liver function tests
low-molecular-weight heparin
lumbar puncture
left ventricular failure
macrophages
m mormng

MAOI 

MAP 

MCA 

MCV 

metab 

MG 

MHRA 

MI 

MMF 

MMSE 

MR 

MRI 

MRSA 

MS 

MTS 

MUST 

monoamine oxidase inhibitor 

mean arterial pressure 

middle cerebral artery 

mean corpuscular volume 

metabolised 

myasthenia gravis 

Medicines and Healthcare Products Regulatory 

Authority (UK) 

myocardial infarction 

mycophenolate mofetil 

Mini-Nlental State Examination (scored out of 30* ) 

modified release (drug preparation)t 

magnetic resonance magmg 

methicillin-resistant Staphylococcus aureus 

multiple sclerosis 

(abbreviated) Mental Test Score (scored out of 10* ) 

malnutrition universal screening tool 

management 

nausea 

NA 

NBM 

NCT 

NDRI 

neb 

NGT 

NH 

NIDDM 

NIHSS 

NIV 

NMJ 

NMS 

NPIS 

NSAID 

nausea and vomiting 

neutrophils 

noradrenaline (norepinephrine) 

sodium (serum levels unless stated otherwise) 

nil by mouth 

narrow complex tachycardia 

noradrenaline and dopamine reuptake inhibitor 

via nebuliser 

nasogastric tube 

non-Hodgkin's (lymphoma) 

non-insulin-dependent diabetes mellitus 

National (US) Institute of Health Stroke Scale 

non-invasive ventilation 

neuromuscular junction 

neuroleptic malignant syndrome 

National Poisons Information Service 

non-steroidal anti-inflammatory drug 

NSTEMI 

NYHA 

OCD 

ocp 

OD 

OGD 

p'way(s) 

PAN 

PBC 

PCI 

PCOS 

PCP 

PCV 

PDA 

PEA 

PEG 

non-ST elevation myocardial infarction 

New York Heart Association 

obsessive compulsive disorder 

oral contraceptive pill 

overdose (NB: od once daily!) 

oesophagogastroduodenoscopy 

pathway(s) 

polyarteritis nodosa 

primary biliary cirrhosis 

percutaneous coronary intervention (now preferred 

term for percutaneous transluminal coronary 

angioplasty (P T CA), which is a subtype of PCI) 

polycystic ovary syndrome 

Pneumocystis carinii pneumonia 

packed cell volume 

patent ductus arteriosus 

pulmonary embolism 

pulseless electrical activity 

percutaneous endoscopic gastrostomy 

PDA 

PEA 

PEG 

PG(x) 

phaeo 

PHx 

PID 

PML 

PMR 

P04 

PPI 

pr 

prep(s) 

prn 

PSA 

PT 

PTSD 

patent ductus arteriosus 

pulmonary embolism 

pulseless electrical activity 

percutaneous endoscopic gastrostomy 

prostaglandin (receptor subtype x) 

phaeochromocytoma 

past history (of) 

pelvic inflammatory disease 

progressive multifocal leukoencephalopathy 

polymyalgia rheumatica 

by mouth (oral) 

phosphate (serum levels, unless stated otherwise) 

proton pump inhibitor 

rectal 

preparation(s) 

as required 

prostate specific antigen 

platelet(s) 

prothrombin time 

parathyroid hormone 

post-traumatic stress disorder 

PUO 

PVD 

QT(c) 

RAS 

RBF 

RLS 

ROSIER 

RRT 

RSV 

RTI 

RV 

RVF 

peptic ulcer 

pyrexia of unknown origin 

peripheral vascular disease 

prophylaxis 

QT interval (corrected for rate) 

rheumatoid arthritis 

renal artery stenosis 

renal blood flow 

renal failure 

restless legs syndrome 

recognition of stroke in emergency room scale for 

diagnosis of stroke/TIA 

respiratory rate 

renal replacement therapy 

respiratory syncytial virus 

respiratory tract infection 

right ventricle 

right ventricular failure 

treatment 

SAH 

SAN 

SBE 

SE(s) 

SIADH 

SIGN 

SJS 

sl 

SLE 

SOA 

SOB (OE) 

SPC 

SPP 

SR 

subarachnoid haemorrhage 

sinoatrial node 

subacute bacterial endocarditis 

subcutaneous 

side effect(s) 

second(s) 

syndrome of inappropriate antidiuretic hormone 

Scottish Intercollegiate Guidelines Network 

Stevens—Johnson syndrome 

sublingual 

systemic lupus erythematosus 

swelling of ankles 

shortness of breath (on exertion) 

summary of product characteristic sheet (see page viii) 

specles 

slow/sustained release (drug preparation)

SSRI 

sss 

STEMI 

supp 

SVT 

tl,'2 

TCA 

TEDS 

TEN 

TFTs 

TIBC 

TIMI score 

TNF 

top 

selective serotonin reuptake inhibitor 

sick sinus syndrome 

ST elevation myocardial infarction 

suppository 

supraventricular tachycardia 

half-life 

triiodothyronine/liothyronine 

thyroxine (T/JT4 = hyper/hypothyroid) 

tricyclic antidepressant 

thromboembolism 

thromboembolism deterrent stockings 

toxic epidermal necrolysis 

thyroid function tests 

triglyceride 

total iron binding capacity 

risk score for UA/NSTEMI named after TIMI 

(thrombolysis in MI) trial 

tumour necrosis factor 

topical 

TPMT 

TPR 

ITA(s) 

TT0(s) 

U&Es 

UA(P) 

UC 

URTI 

VE(s) 

Vlt 

thiopurine methyltransferase 

total peripheral resistance 

(drugs) to take away, i.e. prescriptions for inpatients 

on discharge/leave (aka HO) 

see ITA 

thrombotic thrombocytopenic purpura 

urea and electrolytes 

unstable angina (pectoris) 

ulcerative colitis 

upper respiratory tract infection 

urinary tract infection 

ultraviolet 

vomltlng 

ventricular ectopic(s) 

ventricular fibrillation 

vrtamm 

VLDL 

VTE 

vzv 

w/o 

wcc 

wk 

wkly 

WPW 

Wt 

xs 

ZE 

very-low-density lipoprotein 

ventricular tachycardia 

venous thromboembolism 

varicella zoster virus (chickenpox/shingles) 

with 

within 

without 

white cell count 

Wernicke's encephalopathy 

week 

weekly 

Wolff—Parkinson—White syndrome 

weight 

excess 

Zollinger—Ellison syndrome

Preface ▼xiii
About the authors ▼xvii
Contributors ▼xix
ABCD2 scoring system ▼1
ACE inhibitor-induced cough ▼2
Acetylcysteine for nebulisation ▼3
Acute kidney injury ▼4
Addison’s disease ▼7
Adrenaline: nebulised ▼9
Adverse drug reactions ▼10
Anaemias ▼20
Angioedema: drug causes and treatment ▼25
Antibiotic choice ▼27
Antimicrobial allergy management ▼28
Antiphospholipid syndrome ▼30
Antipsychotics: equivalent doses ▼32
Apomorphine ▼33
Appetite stimulation ▼36
Arterial blood gases and acid–base balance ▼38
Artificial saliva ▼39
Asthma ▼41
Atrial fibrillation ▼47
Bariatric surgery ▼54
Benzodiazepines and ‘z’ hypnotics ▼57
Bicarbonate ▼59
Body surface area calculation ▼61
Bronchiectasis (non-cystic fibrosis) ▼65
Calcium ▼68
Carbamazepine ▼71
Chemotherapy-induced nausea and vomiting ▼74
Child–Pugh score ▼75
Chloramphenicol (systemic) ▼76
Chronic obstructive pulmonary disease ▼79
vii
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Ciclosporin: management and monitoring ▼83
Cigarette smoking: calculation of pack-years ▼86
Cigarette smoking –drug interactions ▼87
Clozapine ▼88
Cognitive assessment
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❦ ❦
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Falls: pharmaceutical care ▼173
Ferinject ▼176
Fluid balance ▼177
Food–drug interactions ▼182
Gastrointestinal bleeding risk management ▼184
Gentamicin ▼185
Glasgow Coma Scale ▼190
Glucosamine ▼192
Grapefruit juice –drug interactions ▼194
Human immunodeficiency virus treatment ▼197
Hyperosmolar hyperglycaemic state ▼208
Hypodermoclysis ▼211
Hypopituitarism ▼213
Ideal body weight ▼216
Immunoglobulin (normal) for intravenous administration ▼216
Inflammatory bowel disease ▼219
Inhaler devices in respiratory disease ▼223
Insulins ▼224
Insulin: variable-rate intravenous insulin infusion ▼231
Interstitial lung disease ▼233
Iron: guidance on parenteral dosing and administration ▼238
Kidney stones (renal calculi) ▼241
Lactose-free medicines ▼243
Learning disability: caring for people with learning disability and
other vulnerable patients ▼244
LipidRescue ▼248
Lithium: management and monitoring ▼249
Liver disease (chronic) ▼253
Liver function tests ▼259
Low-molecular-weight heparin ▼262
Magnesium ▼264
Medicines reconciliation ▼268
Methotrexate: calcium folinate rescue regimen ▼270
Monofer ▼272
Mouth ulcers and sore mouth ▼273
Multiple sclerosis: symptomatic management ▼274
Nausea and vomiting ▼278
Neuroleptic malignant syndrome ▼279
Neutropenic sepsis ▼280
CONTENTS ix
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❦ ❦
❦
Nicotine replacement therapy ▼282
‘Nil-by-mouth’: management of long-term medicines during
surgery ▼284
Nutraceuticals for eye health ▼289
Omeprazole: parenteral administration ▼292
Oncological emergencies ▼296
Opioid comparative doses ▼297
Opioid misuse management ▼298
Opioid partial agonists ▼303
Osteoporosis ▼303
Oxygen ▼308
Pain management ▼311
Palliative and end-of-life care ▼318
Pancreatitis ▼327
Parenteral nutrition: a practical overview ▼331
Patient consultation ▼334
Patient-controlled analgesia ▼339
Phaeochromocytoma ▼341
Pharmacocultural issues ▼343
Phenytoin: management and monitoring ▼345
Phosphate ▼349
Postoperative nausea and vomiting ▼352
Potassium ▼355
Prescription charge exemptions and prepayment certificates ▼360
Protamine ▼361
Prothrombin complex concentrates ▼362
Pulmonary function tests ▼363
Pulmonary hypertension and pulmonary arterial
hypertension ▼368
Quinine for muscle cramps ▼373
Rapid tranquillisation ▼375
Renal disease: assessment of renal function ▼379
Renal disease: dosing in renal impairment and renal replacement
therapy ▼382
Renal disease: chronic kidney disease ▼386
Renal replacement therapy: haemodialysis ▼393
Renal replacement therapy: haemofiltration ▼396
Renal replacement therapy: peritoneal dialysis ▼398
Rheumatoid arthritis: drugs suppressing the disease process ▼400
x CONTENTS
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❦ ❦
❦
Rockall score for gastrointestinal bleed ▼411
Sarcoidosis ▼412
Sclerosants for the management of malignant pleural
effusions ▼415
Serotonin syndrome ▼416
Systemic inflammatory response syndrome due to sepsis scoring
system ▼418
Sodium ▼420
Sterile larvae ▼422
Stroke and transient ischaemic attack ▼424
Suppositories ▼433
Surgical pharmacy ▼434
Synacthen (tetracosactide) tests ▼440
Syndrome of inappropriate secretion of antidiuretic hormone ▼442
Syringe pumps ▼443
Theophylline ▼447
Thunderclap headache ▼450
Thyroid function ▼450
Tinzaparin dosing in pulmonary embolism and deep-vein
thrombosis ▼454
Tobramycin: monitoring and management ▼455
Travel recommendations ▼458
Tuberculosis ▼459
Vancomycin ▼470
Venofer ▼474
Vitamins and minerals ▼474
von Willebrand disease ▼484
Warfarin treatment and monitoring ▼486
Wells score for deep-vein thrombosis ▼494
Wells score for pulmonary embolism ▼495
Yellow Card scheme ▼497
Zinc

high cost of substance addictions

These statistics reflect the dire consequences and high cost of substance addictions only. There are millions more people around the world who suffer from behavioral or activity addictions that are resulting in serious physical, psychological, occupational, financial, interpersonal, and other consequences in their lives. Among these addictions are compulsive eating, gambling, sexual activity, working, exercising, spending, and Internet use—the emphasis being on compulsive. The "war" on drugs has done nothing to end the epidemic of substance abuse. It has only resulted in filling prisons. The prison population in the United States mushroomed from 500,000 in 1980 7 to over two million in 2000.

In India, the lack of fire safety measures snuff out life almost daily why should Hospitals be any different?

In India,  the lack of fire safety measures snuff out life almost daily  why should Hospitals be any different?

In India, hospitals are also tinder boxes where the lack of fire safety measures snuff out life.

 Tuesday, 18 Dec 2018MoneyBusinessTravellerHindi

Calcutta Medical College And Hospital Fire On October 2018, a fire broke out in the dispensary of Says Hospital Had No Fire Clearance the state-run Calcutta Medical College and Hospital. Around 250 patients were evacuated from the building. The eyewitnesses said that there was no disaster management in place to prevent an unfavourable incident. According to reports, faulty electric wiring was the cause of the fire. Bhubaneswar Sum Hospital Fire On October 2016, a major fire broke at Bhubaneswar's Sum Hospital which claimed 22 lives. According to reports, the tragedy occurred due to suffocation as the smoke spread in most of the wards soon after the fire. Most of the victims, who were on oxygen support, died. The most shocking as of the incident was that the security personnel N/A

The most shocking aspect of the incident was that the security personnel prevented dying patients from fleeing the premises, reportedly citing protocol, even pushing them back into the burning building because they had not received orders from the top to release the patients. West Bengal's Murshidabad Medical College Hospital Fire On October 2016, another fire broke out at the West Bengal's Murshidabad Medical College Hospital. Two persons died and seven others were injured in the incident. Cuttack's Shishu Bhawan Hospital Fire On November 2015, a fire broke out at Shishu Bhawan hospital in Cuttack that gutted machines worth Rs 11 lakh, and left one child severely injured. The hospital was already in the news for months over the deaths of several infants due to negligence of doctors. Erwadi Village Mental Home fire In a bone-chilling episode, 28 inmates — bound by chains to trees and beds died after being unable to escape at Moideen Badusha Mental Home in Erwadi Village in Tamil Nadu on August 6, 2001. The faith-based asylum claimed to treat mental illnesses through unique methods. The cause of the fire is N/A

In a bone-chilling episode, 28 inmates — bound by chains to trees and beds died after being unable to escape at Moideen Badusha Mental Home in Erwadi Village in Tamil Nadu on August 6, 2001. The faith-based asylum claimed to treat mental illnesses through unique methods. The cause of the fire is unknown. The charred remains of the dead remain unidentified to date. Bikaner's PBM Hospital Fire Faulty electric wiring caused a fire outbreak at PBM Hospital, Bikaner in January 2013, injuring three infants and damaging property. The wires could not carry the load due to Which the mishap occurred. Kolkata's AMRI Hospital Fire The infamous AMRI hospital fire incident in Kolkata is still afresh. 94 people, 90 of them patients, had died of asphyxiation when inflammable material, stored illegally in an underground car park of one of the wards, caught fire and spread to the upper floors through air conditioner ducts. N/A

Dhananjoy Pal’s daughter was trapped inside the burning hospital, screaming for help, but a guard allegedly prevented her from getting out. “Who will clear your dues?” they asked. The 14-year-old died on the fateful dawn of December 9, 2011, one of the 94 who suffocated when fumes from a fire in the basement of the Advanced Medical Research Ins­titute Hospital (AMRI) in Calcutta’s Dhakuria spread to the upper floors through air conditioning ducts.

For the last seven years, Pal, a resident of Bankura district, has made the grueling 172-km journey to Calcutta and back every single time the courts ann­ounced a hearing in the case of criminal negligence which was filed against the hospital. Seven years on, he’s exhausted and dra­i­ned of resources. “We are middle-class people, without the finances required to pay for lengthy trials. We reposed faith in the legal system. But why does it take so long to get justice?” Pal breaks down, rec­alling his daughter’s premature death. “She was just a child,” he says, his voice quivering with emotion. “If she had lived she would have been 21.” Most relatives of the AMRI fire victims ask the same question. “Why is there no deadline?” Paromita Guha Thakurta, who lost her mother, 64-year-old Mri­dula Devi in the fire, demands.

Immediately after the tragedy, the West Bengal government had swung into action, with chief minister Mamata Banerjee getting the entire top management of AMRI, including its owners and board of directors, arrested. In what was considered an exemplary administrative act, on her instructions, the police filed a chargesheet in just 84 days. In all, 16 officials were charged with cases of criminal negligence, including Section 304 of the Indian Penal Code (culpable homicide not amounting to murder) and Section 304 (attempt to commit culpable homicide), which carry a maximum sentence of life imprisonment and seven years res­pectively. They were also booked under Sections 11C and 11J of the West Bengal Fire Services Act, which pertained to flouting fire safety regulations.

“The proactive role of the state government had reassured victims’ families,” Guha Thakurta says. “But we cannot fathom what transpired subsequently to slow things down.” When, a year later in 2012, the arrested people started to get bail, it disheartened the families. “If the accused were found innocent and acquitted it would not trouble us,” said a relative. “But the trial was still on. Our main concern was that most of the accused being wealthy (several of them are industrialists) they could try to influence the trial. We could not compete with them.”

The aggrieved, exasperated relatives for­med the AMRI Fire Vic­­tims’ Families Association. Its role was to monitor progress in the case and mot­ivate each other to “keep the fight going for justice”. That role it performed doggedly. Raja Ganguly, who lost his 64-year-old father in the fire, flies in from Mumbai, where he works for a pharmaceutical company, to att­end hearings. Others came from Assam, other states and from distant corners of Bengal.

“The travel has been taking its toll on us physically and financially,” says one. “But there doesn’t seem to be light at the end of the tunnel of uncertainty. Justice must be served now, not in the distant future.” The total cost of travel and legal fees has crossed Rs 20-25 lakhs thus far.

THE LUCKY FEW

Rescue workers evacuate people during the AMRI fire on December 9, 2011

PHOTOGRAPH BY AP

Victims’ families say that though they were provided prosecuting law­yers free of cost by the state, most decided to hire the services of legal experts individually. “We don’t doubt their (state prosecutors) efficiency, but in our experience, it is only when we pay that they are really interested.”

Victims’ families bemoan their silent fight. There should have been widespread national outrage, they all feel.

Explains Guha Thakurta, the president of the association, “The accused have hired top legal experts, so we need to ensure that our lawyers are at least equally good.” She rues that, given the gravity of the case, victims’ families stand alone in their resolve. Seven years later, it’s the public apathy that sharpens the families’ sufferings. “It should concern the entire nation, because this was a man-made, public disaster, caused by the negligence of a group of people in whose care we had entrusted our loved ones.” Says Guha Thakurta. “It could have happened to anyone; there should be nat­ional outrage. Why are we forced to fight this as though it was a private matter?” she says, citing the Nirbhaya case, which generated so much anger that it forced Parliament to change the laws.

Guha Thakurta’s mother was admitted for pre-treatment diagnostic tests and was to be released on the night bef­­ore the fire. “Now we live with the regret of not taking her out that very evening.”

Seen through the cold logic of reason, removed from the pain of loss, legal expe­rts explain the delay as inevitable. Cal­cutta advocate Gitanath Gan­guly says, “In legal cases, especially criminal cases, pro­­­­cedural delays cannot be avoided. It is, unfortunately, int­rinsic to the system. For one, dates have to be decided according to the availability of both prosecuting and defence lawyers. Also, our legal system offers legal recourses to petitioners and there are appeals and counter appeals. Moreover, police investigation and witn­ess interrogation etc. are time-consuming processes. These cannot be rushed.”

Indeed, lawyers of the 16 accused in the AMRI case have filed several petitions. For instance, in September 2015, a day after the Supreme Court delivered judgment on the 18-year-old Uphaar case (in 1997, after a fire in Delhi’s Uphaar Cinema killed 59 people, mostly spectators, the owners were charged with criminal negligence) and waived punishment for the accused (in a later judgment in February 2017, the SC sentenced accused Gopal Ansal to a year’s imprisonment), Anindya Mitra, lawyer of AMRI accused and indu­strialist R.S. Agarwal, appealed to the Calcutta High Court that it direct a lower court to hear a plea seeking the quashing of charges against his clients. At that time, the AMRI victims’ families were appealing to the Calcutta HC for a speedy trial, prompting the defence lawyers to plead, in a separate appeal, that their petition be admitted before that of the families’. When asked about the 2015 appeal for exemption, Mitra tells Outlook, “It was for a very specific part of the case.... Beyond that I cannot comment.”

The AMRI case has been heard in seve­ral courts, including lower courts, consumer courts and the sessions court. The case continues in the sess­ions court, with the Calcutta HC monitoring it. Nea­rly 400 witnesses are to be called in for testimony, not to mention the acc­used and relatives of victims. Simultaneous compensation cases were filed by 40 families with the state consumer court; 10 families filed cases in the national consumer court, which was referred to the SC. A source told Outlook that out of 50, 49 consumer cases have been settled.

Ganguly says that even fast-track courts cannot close criminal cases until the judge is thoroughly convinced of the probe and the scrutiny of evidence. On the question of trials being vulnerable to influence, he says, “The wealth, influence and power of the accused is immaterial to the judge. These do not play a role in the deliverance of justice and if they do, these are aberrations and acts of criminality.”

That will provide little succour to relatives nearing the end of their tether, having borne the trauma for each day of these seven years. On December 9, they gathered for a memorial service for their dep­arted relatives. Along with prayers for their souls to rest in peace, a deepening sense of unease permeated their beings.

***

Days after fire, 16 arrested, remanded in custody, chargesheet filed, trial starts. Speedy trial demanded in HC in 2013.Case in Sessions Court in 2013. Referred to HC, which monitors it. Accused’s appeal for quashing of charges denied by courts.In 2016, all 16 charged under IPC sections, including culpable homicide. Case insessions court; next hearing: Jan 8, 2019.

Solving primary care shortage.The solution is simple close all Medical colleges in USA and open more Nurse practitioner schools

  One study after another is being published showing that, Nurse practitioners do a better job than Physicians in taking care of patients.

Some observers argue that physicians are overqualified for some of today's primary care work, which can involve routine physical assessments and ongoing care rather than diagnosis and treatment of complex conditions.

In 2012, 18 states and the District of Columbia allowed nurse practitioners to diagnose and treat patients and prescribe medications without a physician's involvement, while 32 states required physician involvement to diagnose and treat or prescribe medications, or both .

First step make it mandatory for all the legislators who passed theses laws to obtain their care only from  Nurse practitioners.

Second step convert all the medical schools in theses states in to  Nurse practitioner schools.

Third step: Do a detailed study  and  amalgamate the NP training  with basic medical degree training to create a hybrid practitioner curriculum and provide openings for all takers who are able to pass minimum requirements.


Roughly 5,700 geographic areas containing 55 million residents as being Primary Care Health Professional Shortage Areas.
shift all the present  medical schools to these areas. and convert all the present  medical schools to the new hybrid course

CHC_Epidemiology of HIV Overview

Topic 1HIV Prevalence approximately 13% remain undiagnosed. hence slightly underestimatedESTIMATED HIV PREVALENCEThis graph shows CDC estimates for persons ≥13 years old living with diagnosed or undiagnosed HIV infection in the United States during the years 2007-2013.Figure 1. Estimated HIV Prevalence in United States, 2007-2013*The CDC estimates that 1,242,400 persons 13 years of age and older were living with HIV infection in the United States at the end of 2013, including 1,080,800 persons with diagnosed HIV infection and 161,200 with undiagnosed HIV infection. The number of persons living with HIV (prevalence) in the United States increased each year from 2007 to 2012 (Figure 1), because the number of new HIV infections per year outpaced the number of persons with HIV/AIDS who died per year.The Government of India estimates that about 2.40 million Indians are living withHIV (1.93 ‐3.04 million) with an adult prevalence of 0.31% (2009). Children (<15 15-49="" 3.5="" 83="" account="" age="" all="" are="" for="" group="" in="" infections="" of="" span="" the="" while="" years.="" yrs="">HIV infections, 39% (930,000) are among women.

2Topic 2Newly Diagnosed with HIV InfectionIn the United States, for the year 2015, an estimated 39,513 persons were newly diagnosed with HIV infection (any stage of HIV disease).[1] The number of new HIV diagnoses has declined 10% from 2010 to 2015, suggesting a true trend in declining new infections .. The rate of new HIV diagnosis in 2015 was 12.3 per 100,000 population.
In 2016, India had 80 000 (62 000 - 100 000) new HIV infections and 62 000 (43 000 - 91 000) AIDS-related deaths. There were 2 100 000 (1 700 000 - 2 600 000) people living with HIV in 2016, among whom 49% (40% - 61%) were accessing antiretroviral therapy.

Topic 3Undiagnosed HIV Infection

UNDIAGNOSED HIV IN THE UNITED STATES

Figure 13. Proportion of Persons with Undiagnosed HIV Infection in United Sates, 2007-2013

Using back-calculation methods,[8] the CDC estimated at the end of 2013, 13% of persons living with HIV infection had undiagnosed HIV.[2] From 2003 to 2006 the percentage of persons with undiagnosed HIV infection in the United States declined from approximately 25% to 17%; since 2007 the undiagnosed fraction of persons living with HIV has continued to further decline, although in the last several years the undiagnosed fraction has leveled off at approximately 13% (Figure 13).[2,3,8,9,10] Persons unaware of their HIV status are unable to benefit from treatment of their HIV infection and are more likely to transmit HIV to others

HIV testing and treatment cascadePeople living with HIV 2 100 000 [1 500 000 - 3 000 000]People living with HIV who know their status 1 700 000Percent of people living with HIV who know their status 79 [56 - >95]People living with HIV who are on ART 1 200 000Percent of people living with HIV who are on ART 56 [40 - 79]People living with HIV who have suppressed viral loads ...

4Topic 4HIV Incidence Estimates

Knowledge about HIV prevention among young people aged 15-24	26.17
Knowledge about HIV prevention among young women aged 15-24	21.7
Knowledge about HIV prevention among young men aged 15-24	31.5

5Topic 5Social Determinants of Health and HIV

6Topic 6Deaths in Persons with HIV Infection

7Topic 7Global HIV-1 Epidemiology

8Topic 8HIV-2

9Topic 9Summary Points

CECNE and CME QuizEpidemiology of HIV CE Quiz