clw 8 Flashcards

HF, hepatitis, liver cirrhosis, asthma, VTE

1
Q

name 3 differential causes of dyspnoea

A
  • fluid overload secondary to hfref
  • asthma
  • pulmonary embolism
  • pneumonia
  • lung cancer
  • MI
  • ascites due to liver cirrhosis
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2
Q

main sx of fluid overload secondary to HF

A

Orthopnoea - cannot breathe when lying down at night

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3
Q

telltale sx of ascites due to liver cirrhosis causing dyspnoea

A

palmar erythema
jaundice, ascites
pruritis
spider angiomata

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4
Q

lab results to look out for when liver has issues

A

elevated lft
coagulation tests (PT, aPTT, INR)

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5
Q

asthma sx

A

wheezing (auscultation)
SOB
chest tightness
unable to talk in sentences
elevated pulse rate

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6
Q

pulmonary embolism s/sx

A

d-dimer
unilateral pitting edema (dvt)

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7
Q

ssx of pneumonia

A

fever
cxr lung consolidation
chest pain

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8
Q

s/sx of MI

A

chest pains
elevated heart rate
palpitations
diaphoresis (excess sweat)
elevation in cardiac troponin
ST elevation? ECG abnormalities

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9
Q

GOT for HF

A

resolve fluid overload (0.5kg weight loss/day)
optimise HF therapy to prevent complications and reduce mortality risk
improve exercise capacity

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10
Q

when increasing furosemide for fluid overload episode, how much to increase?

A

double home dose or switch to IV (of same dose)

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11
Q

BD dosing for diuretic should not be at night to_

A

prevent need for pt to wake up at night to pee

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12
Q

always start with IV for episodes of fluid overload requiring hospitalisation at how much dose?

A

at same IV dose

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13
Q

what do beta blockers do

A

decrease HR and cardiac output

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14
Q

if patient is hemodynamically unstable, what to do with F4 agents

A

continue but maintain same dose

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15
Q

when to hold off SGLT2i

A

before surgery, in acute illness. not for fluid overload

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16
Q

what are the agents for HF

A

spironolactone
sglt28
arni/acei
bb
+
diuretic

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17
Q

first line for ascites

A

spironolactone, furosemide

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18
Q

when to hold use of bb

A

HR low

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19
Q

non pharm of HF

A

lose weight
restrict Na (<2g/d) and water (800-1L)
remove K from veg
weigh daily to monitor for fluid issues
cardiac rehab program and exercise

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20
Q

what to monitor for diuretic use

A

serum k, Na, Cr
genital infections

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21
Q

uses of f4 agents

A
  • relieve/reduce sx
  • reduce need for admissions
  • prolong survival
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22
Q

GOT of ascites with liver cirrhosis

A
  • managing sx and normalising liver abnormalities
  • slowing down disease progression
  • preventing complications of liver cirrhosis
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23
Q

GOT of viral hep B

A

viral suppression

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24
Q

GOT of hep C

A

viral eradication

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25
Q

what to do before treating hep b

A

screen for hiv

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26
Q

main side effect of concern for arni/acei

A

hypotension

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27
Q

bb for HF

A

bisoprolol, carvedilol (but not selective), metoprolol XL

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28
Q

how to manage portal htn

A

propranolol, nadolol, carvedilol
endoscopic variceal ligation (EVL)

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29
Q

nonpharm of ascites/cirrhosis

A
  • drain out ascitic fluid
  • abstain from alcohol
  • salt restriction
  • avoid nsaid, acei
    *fluid restriction not necessary unless serum Na ≤125mmol/L
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30
Q

non pharm hepatitis b

A
  • prevent disease transmission (household contacts shd b vaccinated)
  • do not donate blood
  • weight loss
  • avoid alcohol and smoking
  • inform healthcare providers of the condition
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31
Q

spironolactone se

A

gynaecomastia, hyperK

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32
Q

how to monitor asthma control

A

ACT questionnaire

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33
Q

why can’t use saba alone

A

increased risk of exacerbations and hospitalisation

downregulates beta receptors in lungs, reduce responsiveness, affect long term control

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34
Q

administration technique for ics-laba

A

use everyday even if well controlled
wash mouth after using to prevent oral thrush

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35
Q

non pharm for asthma / copd

A
  • avoid triggers eg tobacco, allergens
  • exercise/breathing exercises
  • avoid use of nsaids, bb
  • update vaccinations
  • remediation of dampness or mould in homes
  • dealing with emotional stress
  • (copd) nutritional support
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36
Q

what is pulmonary rehab prog for copd

A

patient education, exercise trng, nutritional support, psychosocial support

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37
Q

vaccination in copd

A

pneumococcal: PCV13 and PPSV23
influenza

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38
Q

how to monitor asthma

A

symptoms of exacerbation, frequency of exacerbation and use of inhaler

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39
Q

what to always monitor fo HTN drugs

A

serum creatinine

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40
Q

benefit for sglt2i and loops used together

A

natriuresis effect - kidneys excrete sodium

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41
Q

how does liver cirrhosis affect drug distribution

A

decreased albumin pdtn. affects protein binding and amt of unbound drug

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42
Q

how does liver cirrhosis affect cyp enzyme

A

cyp expression reduced, decreased metabolism of drug, longer half life /elimination of drug

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43
Q

what is formula of hepatic extraction ratio

A

E = 1-F

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44
Q

what happens to drug when reduced hepatic blood flow

A

less drug brought to liver for metabolism, decreased clearance

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45
Q

high extraction ratio

A

> 0.7

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46
Q

when drug has high extraction ratio, is it perfusion limited? is it sensitive to changes in perfusion or protein binding?

A

yes. perfusion

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47
Q

when drug has low extraction ratio, is it perfusion limited? is it sensitive to changes in perfusion or protein binding?

A

no, protein binding

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48
Q

in cirrhosis, for drugs of high extraction ratio, do you have to reduce initial/maintenance dose?

A

yes both. affected greatly by extent of metabolism of liver. first past effect evident
maximal plasma concentration and F is increased, elimination is slowed.

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49
Q

in cirrhosis, for drugs of low extraction ratio, do you have to reduce initial/maintenance dose?

A

only maintenance dose. only elimination is slowed

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50
Q

what do drugs in bile undergo (2 ways)

A

1) enterohepatic cycling -reabsorption
2) excreted via feces

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51
Q

characteristics of drugs secreted into bile

A
  • polar
  • MW > 350g/mol
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52
Q

main side effect of statins

A

hepatic enzymes elevation, myalgia

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53
Q

estrogen metabolism

A

liver

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54
Q

obesity: serum albumin?

A

same

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55
Q

obesity: liver blood flow

A

may increase

56
Q

obesity: cyp3a4? (phase 1)

A

decrease

57
Q

obesity: gastric emptying

A

increase

58
Q

obesity: oral F

A

largely the same

59
Q

renal clearance in obesity

A

increase then decrease

60
Q

obesity: adipose tissue

A

increased

61
Q

obesity: gut permeability

A

increase

62
Q

what protein is increased in obesity

A

alpha one glycoprotein

63
Q

obesity: cyp2e1 (phase I)

A

increased

64
Q

phase 2 in obesity

A

increased glucuronidation and sulfation

65
Q

alpha 1 glycoprotein binds more to acidic or basic drugs?

A

basic

66
Q

albumin binds more to acidic or basic drugs?

A

acidic. albumin is basic

67
Q

obesity: cardiac output?

A

increase

68
Q

obesity related kidney problem

A

obesity-related glomerulopathy

69
Q

when to use adjusted BW

A

aminoglycosides dosing. AG is hydrophilic with low Vd

70
Q

dvt wells score? confirm dvt

A

at least 2 pts

71
Q

if wells score less than 2? conduct d dimer. what does d dimer show?

A

negative: no dvt
positive: maybe dvt

72
Q

DOACs under crcl_ cannot use

A

30, switch to enox or warfarin

73
Q

GOT for DVT

A

prevent extension of embolisation of thrombus (ie escalation to PE)
relieve symptoms
prevent recurrence

74
Q

when starting sglt2i for HF, what should be stopped

A

IV diuretic

75
Q

which sglt2is are useful in hfref

A

dapa and empa

76
Q

uses of sglt2i in hfref

A
  • reduces hospitalisation due to new HF
  • reduce onset of new HF for ppl with high CVS events
77
Q

what is used as adjunct to bb?

A

ivabradine

78
Q

how does ivabradine help in hf?

A

prolong survival, relieve symptoms, prevent admissions

79
Q

if switching from acei to arni, wash out period how long

A

36h

80
Q

when adding loop diuretics, watch out for what

A

K/RP (hypokalemia)
maybe give potassium chloride replacement

81
Q

sglt2i watch out for what

A

euglycemic diabetic ketoacidosis, genitourinary tract infections

82
Q

EDKA symptoms

A

malaise, vomiting, dyspnea, nausea

83
Q

why do raasi agents cause hyperk

A

they retain potassium

84
Q

counselling points for BB in HF

A
  1. Some px could take 3-6 months before experiencing an improvement
  2. There could be an initial worsening before improvement
  3. It is important to measure body weight daily
85
Q

target hr in hfref

A

below 70

86
Q

when starting sglt2i must make sure SBP_?

A

> 100

87
Q

treatment for chronic hep c

A

Anti-HCV Nucleoside Agent (NA)- Ribavirin

88
Q

side effects of chronic hep c tx

A

Haemolytic anaemia
Fatigue
Teratogenic

89
Q

what are useful markers of liver disease

A

ALP, AST, ALT (GGT alone not useful)

90
Q

features of viral hepatitis

A

fever, nausea, vomiting, pale stools, jaundice

91
Q

what does liver cirrhosis result in

A
  • portal htn
  • varices
  • decrease in albumin levels
  • impedes portal blood flow
  • hepatocellular carcinoma
  • encephalopathy (disturbance to brain fx)
92
Q

how does decreased albumin synthesis lead to ascites

A

changes in intravascular oncotic pressure

93
Q

how does underfilling of circulation lead to ascites

A

combined with reduced aldosterone metabolism, leads to activation of RAA system

94
Q

GOT of portal hypertension

A

prevention of bleeding

95
Q

how does cirrhosis affect coagulation

A

Decreased synthesis of most procoagulant factors as well as naturally occurring
anticoagulants, antithrombin, protein C and S

96
Q

nonalcoholic fatty liver disease risk factors

A

obesity, diabetes

97
Q

why need to check ascitic fluid

A

spontaneous bacterial bacterial peritonitis (infection of ascitic fluid)

98
Q

primary prophylaxis for who

A
  • child pugh c small varices
  • big varices
99
Q

propranolol therapy goal

A

resting HR 55-60/min
sbp > 90mmhg

100
Q

in patients with asthma, what is the issue of BB?

A

beta 2 found in lungs, blocking receptors can increase risk of bronchospasms

101
Q

antibiotic prophylaxis for acute variceal bleed

A

ceftriaxone, norfloxacine

102
Q

vasoactive agents in portal htn for ?

A

inhibit splanchnic vasodilation
eg. octreotide, vasopressin, SMT, telipressin

103
Q

secondary prophylaxis of portal htn?

A

nsbb and chronic evl

104
Q

GOT for hepatic encephalopathy

A

reduce ammonia blood concentration

105
Q

non pharm for hepatic encephalopathy

A

diet: protein restriction
supplement with elemental zinc

106
Q

pharm for hepatic enceph

A

lactulose: lower colonic pH, promotes conversion of ammonia to ammonium for excretion

rifaximin: targets anaerobic bacteria that produce urease which hydrolyzes urea to ammonia in gut

107
Q

non-alcoholic fatty liver (NAFL) vs non-alcoholic steatohepatitis (NASH)

A

NAFL: no evidence of hepatocellular injury, minimal risk of progression to cirrhosis

NASH: inflammation and hepatocellular injury, may progress to cirrhosis and liver failure

108
Q

GOT of asthma

A
  • reduce need for reliever medication
  • avoid troublesome symptoms esp at night
  • avoid serious asthma flare-ups
  • to achieve good control of
    symptoms and maintain normal activity levels
109
Q

benefits of addition of laba to ics

A

decreases nocturnal asthma, use of rapid-acting b2 agonist and number of exacerbations

110
Q

diagnosing asthma

A

fev1/fvc is <0.7

111
Q

what is fev1

A

volume of air exhaled forcefully in first second of maximal expiration

112
Q

fvc

A

Maximum amount of air
that can be exhaled when
blowing out as fast as
possible, after full
inspiration

113
Q

increase of fev1 after saba to show asthma?

A

≥12%

114
Q

tcu of asthma

A

3-6 months after treatment changes; every 1-2 years if stable

115
Q

host risk factors for asthma

A

Genetic predisposition
* Atopy
* Gender
* Obesity

116
Q

environmental factors for asthma

A

Indoor allergens
* Outdoor allergens
* Occupational
sensitizers
* Tobacco smoke
* Air Pollution
* Respiratory Infections
* Socioeconomic
factors
* Diet

117
Q

risk factor for exacerbation

A
  • History of ≥1
    exacerbations
    in the previous
    year
  • Poor
    adherence
  • Incorrect
    inhaler
    technique
  • high saba use
118
Q

benefits of low dose ics (in asthma)

A

– Markedly reduces asthma deaths
– Reduces hospitalizations
and readmissions
– Prevents exacerbations
– Protects against long-term decline in lung function

119
Q

benefit of ics in copd

A

improve lung fx and oxygenation
shorten length of hospital stay
decrease relapse and treatment failure rates

120
Q

IC steroids monitor for what

A

osteoporosis, oral thrust, cough, adrenal suppression, HTN, diabetes

121
Q

after an exacerbation, review within

A

1w

122
Q

consider step down after good control maintained for

A

3 months

123
Q

MOA of montelukast

A
  • Interfere in the release of leukotriene mediators from mast cells,
    eosinophils and basophils
  • Reduce symptoms associated with the inflammatory allergic
    component of asthma, including swelling of the airway and smooth
    muscle constriction
124
Q

adr of montelukast

A

Headache, nausea
Neuropsychiatric events

125
Q

theophylline

A

induces SM relaxation via inhibition of phosphodiesterase 3, leading to bronchodilation

126
Q

adr of theophylline

A

 GI: nausea, vomiting
 CNS: insomnia, headache, seizures
 Cardiac: tachycardia, cardiac flutter

127
Q

emphysema in copd

A
  • Abnormal permanent
    enlargement of the airspaces
    distal to terminal bronchioles
  • Accompanied by destruction
    of their walls ± obvious
    fibrosis
128
Q

copd primarily due to

A

exposure to noxious particles or gases

129
Q

risk factors of copd

A

tobacco smoking
air pollution
occupational exposures
female
age

130
Q

copd clinical presentation

A

dyspnea, chronic cough, sputum production
wheezing, chest tightness, fatigue, weight loss, anorexia
age>40

131
Q

copd symptoms use what scoring

A

mMRC or CAT

132
Q

mMRC scale 0-4

A

0 - least sx; 4 - too breathless to leave house

133
Q

CAT

A

scale of 0 to 40, >30 is high impact on life

134
Q

GOT for COPD

A

relieve symptoms, improve exercise tolerance
prevent disease progression and mortality

135
Q

uses of LABA and LAMA in copd

A

improve lung fx, dyspnea, health status, reduce exacerbation rates

136
Q

long term steroid use can be associated with

A

risk of pneumonia and mortality

137
Q

over use of abx in copd can lead to

A

spread of resistant organisms