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AGM 2 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

osmolarity

A

number of solute particles per liter

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2
Q

osmolality

A

number of solute particles per kg

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3
Q

where are baroreceptors located

A

kidneys, atria, pulmonary veins, carotids, aortic arch

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4
Q

what do baroreceptors detect

A

changes in pressure and volume

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5
Q

what do baroreceptors do in response to large changes

A

signal posterior pituitary to release ADH

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6
Q

osmoreceptors location

A

hypothalamus

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7
Q

what happens in response to osmolality changes

A

release of ADH

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8
Q

what is true of osmoreceptors in elderly

A

they are sensitive

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9
Q

what percentage by weight does water make up in the elderly

A

50%

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10
Q

fraction of total body water that is ICF

A

2/3

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11
Q

fraction of total body water that is ECF

A

1/3

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12
Q

fraction of ECF that is interstitial

A

2/3

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13
Q

fraction of ECF that is plasma

A

1/3

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14
Q

most common electrolyte imbalance in hospital

A

hyponatremia

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15
Q

complication of correcting hyponatremia too quickly

A

death

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16
Q

ssx of severe hyponatremia

A

stupor/coma, seizures, respiratory arrest

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17
Q

ssx of mild-advancing hyponatremia

A

headache, irritability, N/V, AMS, ataxia

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18
Q

main categories of causes of hypovolemic hyponatremia

A

renal or extrarenal losses

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19
Q

causes of renal losses in hypovolemic hyponatremia

A

diuretic excess, mineralocorticoid deficiency, renal tubular acidosis, osmotic diuresis (hyperglycemia, uremia etc)

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20
Q

causes of extrarenal losses in hypovolemic hyponatremia

A

vomiting, diarrhea, burns, trauma, pancreatitis

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21
Q

urinary sodium concentration in renal vs extrarenal losses in hypovolemic hyponatremia

A

renal: >20 mmol/l
extrarenal: <10 mm/l

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22
Q

hypovolemic hyponatremia treatment

A

isotonic saline

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23
Q

what is euvolemic hyponatremia

A

elevated total body water with a normal total body sodium

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24
Q

causes of euvolemic hyponatremia

A

glucocorticoid deficiency, hypothyroidism, pain, psych, drugs, SIADH

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25
Q

urinary sodium concentration in euvolemic hyponatremia

A

> 20 mmol/l

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26
Q

euvolemic hyponatremia treatment

A

fluid restriction

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27
Q

what is hypervolemic hyponatremia

A

greatly elevated total body water and elevated total body sodium

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28
Q

causes of hypervolemic hyponatremia

A

nephrotic syndrome, heart failure, cirrhosis, acute/chronic renal failure

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29
Q

urinary sodium concentration in hypervolemic hyponatremia

A

acute/chronic renal failure: >20 mmol/l. all other causes: <10 mmol/l

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30
Q

hypervolemic hyponatremia treatment

A

fluid and sodium restriction

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31
Q

where is dietary potassium absorbed

A

intestines

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32
Q

where is potassium excreted

A

distal tubule

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33
Q

what facilitates intracellular uptake of potassium

A

insulin

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34
Q

hormonal consequences of hyperkalemia

A

stimulates secretion of aldosterone

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35
Q

causes of hypokalemia

A

loop diuretics, albuterol, vomiting, diarrhea, hyperinsulinemia

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36
Q

ssx of hypokalemia

A

muscle weakness, arrhythmias

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37
Q

ECG changes in hypokalemia

A

u waves, flattened T-waves

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38
Q

causes of hyperkalemia

A

CKD, hyperglycemia, hyperosmolality (why?) insulin (why?), beta blockers (?), rhabdo

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39
Q

ssx of hyperkalemia

A

muscle weakness, paralysis, arrhythmias, bradycardia

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40
Q

ECG changes in hyperkalemia

A

peaked T-waves, widened QRS

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41
Q

name of grading system for ulcers

A

Wagner

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42
Q

Wagner grade 2 ulcer

A

involves ligament, tendon, joint capsule, or fascia without abscess or osteomyelitis

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43
Q

Wagner grade 3 ulcer

A

deep ulcer with abscess or osteomyelitis

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44
Q

Wagner grade 4 ulcer

A

gangrene to forefoot

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45
Q

Wagner grade 5 ulcer

A

extensive gangrene

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46
Q

Wells criteria high risk

A

greater than or equal to 3

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47
Q

Wells criteria moderate risk

A

1-2

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48
Q

Wells criteria low risk

A

less than 1

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49
Q

Wells criteria components

A

active cancer, stasis, bedridden due to surgery, deep vein tenderness, entire leg swollen, unilateral calf swelling/pitting edema, prior history of DVT/PE

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50
Q

edema type: predilection for medial ankle/calf

A

venous insufficiency

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51
Q

edema type: tender with positive Homans sign

A

DVT

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52
Q

edema type: early pitting, late fibrotic/hyperkeratotic

A

lymphedema

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53
Q

edema type: nonpitting, affecting legs but sparing ankles and feet

A

lipedema

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54
Q

edema type: associated with weeping ulcerations over medial malleolus

A

venous insufficiency

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55
Q

edema type: associated with hemosiderin deposition

A

venous insufficiency

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56
Q

edema type: Inability to tent skin over second digit

A

lymphedema

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57
Q

edema type: warmth over affected extremity

A

DVT or cellulitis

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58
Q

edema type: associated with lipodermatosclerosis

A

venous insufficiency

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59
Q

edema type: nonpitting, generalized, periorbital, yellow-orange skin discoloration over knees, elbows, palms, soles

A

myxedema

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60
Q

Kaposi-Stemmer sign

A

inability to tent skin over second digit

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61
Q

edema type: prominent malleolar fat pads

A

lipedema

62
Q

May-Thurner syndrome

A

compression of the left iliac vein by the right iliac artery in young women causing edema of the LLE

63
Q

likely etiology of edema in obstructive sleep apnea

A

pulmonary hypertension (does not explain all cases)

64
Q

treatment for mild venous insufficiency

A

compression stockings at 20-30 mmHg

65
Q

treatment for moderate-severe venous insufficiency

A

compression stockings at 30-40 mmHg

66
Q

compression stocking contraindication

A

PAD (must be careful because venous insufficiency may coexist with PAD)

67
Q

how to assess for PAD

A

ankle-brachial index

68
Q

edema type: associated with stasis dermatitis

A

venous insufficiency

69
Q

treatment for stasis dermatitis

A

topical steroids and emollients

70
Q

treatment for lymphedema

A

manual lymphatic massage, compression at 30-40 mmHg, pneumatic compression devices

71
Q

what is post-thrombotic syndrome

A

chronic leg swelling, cramping, pain, skin changes in those with prior DVT

72
Q

how to prevent post-thrombotic syndrome

A

use compression stockings in addition to anticoagulants for DVT

73
Q

what is factor V leiden

A

hypercoagulable state and increased thrombin generation caused by genetic defect leading to inability to break down factor V

74
Q

how is factor V leiden diagnosed

A

activated protein C, genetic testing, others

75
Q

what antibodies can be elevated in the case of thrombisis

A

antiphospholipid antibodies

76
Q

protein C and S functions

A

work as part of natural anticoagulant system

77
Q

causes of protein C and S deficiency

A

genetic, liver disease, warfarin, malnutrition, autoimmune disorders (S only), active clotting states (eg venous thrombosis)

78
Q

what is antithrombin III

A

a globulin produced in liver that inhibits coagulation, provides most of the anticoagulant effect of heparin

79
Q

causes of antithrombin III deficiency

A

genetic, liver disease, malignancy, DIC, acute thrombosis, nephrotic syndrome

80
Q

at what percentage of occlusion do symptoms appear in PAD

A

70%

81
Q

PAD pain in hips/buttocks

A

aorta or iliac artery involvement

82
Q

PAD pain in thigh

A

iliac/common femoral artery involvement

83
Q

PAD pain in upper 2/3 of calf

A

superficial femoral artery

84
Q

PAD pain in lower 1/3 of calf

A

popliteal artery involvement

85
Q

PAD pain in lateral calf (per Laura)

A

tibial artery involvement

86
Q

pathophys of ischemic ulcers

A

start as small traumatic wounds and have insufficient blood supply for healing

87
Q

ischemic ulcers location

A

pressure points, malleoli, toe joints, shin

88
Q

ischemic ulcers presentation

A

dry, punched-out, painful, little bleeding

89
Q

normal ABI range

A

1.0-1.4

90
Q

borderline ABI range

A

0.91-0.99 (can proceed to exercise testing)

91
Q

false negative ABI range

A

> 1.4 (can proceed to toe brachial index)

92
Q

severe PAD ABI range

A

<0.4

93
Q

mild-moderate PAD ABI range

A

0.4-0.9

94
Q

gold standard for PAD imaging

A

conventional arteriography

95
Q

usual 1st-line advanced imaging for PAD

A

CT angiography

96
Q

components of Virchow’s triad

A

stasis, hypercoagulability, endothelial injury

97
Q

what is best anticoagulant choice in elderly

A

DOACs (rivaroxaban, apaxiban)

98
Q

advantages of DOACs

A

easy to monitor, short half-life

99
Q

how much delay until onset of action for vit k antagonists and why

A

5 days because of half-life of previously formed coag factors

100
Q

how long to continue heparin bridge

A

for 5 days after starting vit k antagonist and until INR is within target range for 24 hours

101
Q

recommended duration of anticoagulation after first instance of VTE due to reversible risk factor

A

3 months

102
Q

recommended during of anticoagulation after first instance of unprovoked VTE not attributable to reversible risk factor

A

lifelong if low or moderate bleeding risk, 3 months if high bleeding risk

103
Q

when can a VTE not involve anticoagulation

A

if mild distal DVT without severe symptoms, may use serial monitor instead of anticoagulation for first two weeks

104
Q

what should patients do after completion of anticoagulation course?

A

take aspirin lifelong

105
Q

if VTE recurrence while on vit K antagonist or DOAC

A

switch to LMWH

106
Q

when should INR be obtained when initiating vit k antagonist therapy

A

baseline, after 2-3 doses, then twice weekly until INR is in therapeutic range. Then weekly, every other week, and then monthly. Can be q 12 weeks once Pt has stable INR for 3 months

107
Q

what to do if INR<4.5 but greater than goal

A

hold dosage and resume at a lower dose once INR is within therapeutic range

108
Q

what to do if INR is 4.5-10

A

hold the next 1-2 doses, increase monitoring, resume at lower dose once INR is within range

109
Q

what to do if INR is >10

A

administer vitamin K, increase monitoring, and continue administering vitamin K if needed. Resume vit K antagonist at appropriate dosage when INR returns to therapeutic range

110
Q

timing of vit k antagonist dosage

A

should be taken at the same time every day

111
Q

components of CHADS2

A

CHF, HTN, Age over 75, DM, prior Stroke

112
Q

which DOAC confers higher risk of GI hemorrhage

A

rivaroxaban

113
Q

elements of HAS-BLED

A

HTN, Abnormal renal function, Stroke, Bleeding, Labile INR, Elderly, Drugs/alcohol

114
Q

DOAC half-life

A

approx 12 hours

115
Q

Beta 1 selective drugs

A

metoprolol, atenolol, esmolol

116
Q

key side effect of clonidine

A

rebound HTN

117
Q

main effect of dihydropyridine CCBs

A

vasodilation

118
Q

ACE I’s and ARBs can cause what electrolyte disturbance

A

hyperkalemia

119
Q

majority of PAD obstructions location

A

popliteal artery

120
Q

beri beri

A

thiamine deficiency

121
Q

main cause of lymphedema industrialized world

A

cancer

122
Q

why does renal failure cause edema

A

fluid overload, protein loss via glomerulus, oversecretion of renin

123
Q

edema type thin skin tight with water

A

protein malnutrition

124
Q

medications causing edema

A

steroids, hormones, NSAIDs, CCBs (peeeeens)

125
Q

“hormonal cascade of death”

A

obstructive sleep apnea

126
Q

pitting edema grading scale

A

0-4

127
Q

Leriche Syndrome

A

ED, aorto-iliac PAD, ass pain

128
Q

drugs for PAD

A

statins, ASA, ACE-inhibitors, plavix, pletal (cilostazol)

129
Q

congenital primary lymphedema

A

Milroy (born without lymph nodes)

130
Q

primary lymphedema in females 1-35 y/o

A

lymphedema praecox (Meige disease)

131
Q

what is horse chestnut seed extract for

A

venous insufficiency

132
Q

what is peau dorange associated with

A

lipedema

133
Q

what type of afib requires warfarin

A

valvular

134
Q

goal INR for warfarin

A

2-3

135
Q

muscle holds how much ICF

A

75%

136
Q

what percent of ECF is in veins

A

85%

137
Q

effective osmoles

A

Na, glucose

138
Q

ineffective osmoles

A

alcohols, lipids, proteins

139
Q

drug triggers for ADH release

A

NSAIDs, SSRIs, cancer drugs, seizure meds, tumors

140
Q

pseudohyponatremia

A

some interfering factor causing a false hyponatremia (lipids, proteins, urea, immunoglobins)

141
Q

severe hyponatremia cutoff

A

under 120

142
Q

where is potassium excreted

A

distal tubule

143
Q

thiazide diuretics side effects

A

hypokalemia, hyperlipidemia, hyperglycemia, hypercalcemia, hyperuremia

144
Q

criteria for orthostatic hypotension

A

decrease of 20 mmHg systolic or 10 mmHg diastolic within 3 minutes of standing

145
Q

thiazides mechanism of action

A

inhibit sodium reabsorption in distal convoluted tubule

146
Q

what part of nephron do carbonic anhydrase inhibitors affect

A

proximal convoluted tubule

147
Q

what must be monitored in patients taking loop diuretics

A

potassium and creatinine

148
Q

effects of angiotensin II

A

vasoconstriction, aldosterone release, increases Na resorption, stimulates thirst, stimulates release of ADH

149
Q

effects of aldosterone

A

increases Na resorption (slower than angiotensin II because it is a hormone)

150
Q

when is pharmacologic intervention for HTN recommended

A

> 10% 10 year risk and BP>130/80

151
Q

electrolyte imbalance that can occur with ACEI

A

hyperkalemia

AGM 2 (4 decks)

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