Exam 2 Flashcards
(151 cards)
1
Q
osmolarity
A
number of solute particles per liter
2
Q
osmolality
A
number of solute particles per kg
3
Q
where are baroreceptors located
A
kidneys, atria, pulmonary veins, carotids, aortic arch
4
Q
what do baroreceptors detect
A
changes in pressure and volume
5
Q
what do baroreceptors do in response to large changes
A
signal posterior pituitary to release ADH
6
Q
osmoreceptors location
A
hypothalamus
7
Q
what happens in response to osmolality changes
A
release of ADH
8
Q
what is true of osmoreceptors in elderly
A
they are sensitive
9
Q
what percentage by weight does water make up in the elderly
A
50%
10
Q
fraction of total body water that is ICF
A
2/3
11
Q
fraction of total body water that is ECF
A
1/3
12
Q
fraction of ECF that is interstitial
A
2/3
13
Q
fraction of ECF that is plasma
A
1/3
14
Q
most common electrolyte imbalance in hospital
A
hyponatremia
15
Q
complication of correcting hyponatremia too quickly
A
death
16
Q
ssx of severe hyponatremia
A
stupor/coma, seizures, respiratory arrest
17
Q
ssx of mild-advancing hyponatremia
A
headache, irritability, N/V, AMS, ataxia
18
Q
main categories of causes of hypovolemic hyponatremia
A
renal or extrarenal losses
19
Q
causes of renal losses in hypovolemic hyponatremia
A
diuretic excess, mineralocorticoid deficiency, renal tubular acidosis, osmotic diuresis (hyperglycemia, uremia etc)
20
Q
causes of extrarenal losses in hypovolemic hyponatremia
A
vomiting, diarrhea, burns, trauma, pancreatitis
21
Q
urinary sodium concentration in renal vs extrarenal losses in hypovolemic hyponatremia
A
renal: >20 mmol/l
extrarenal: <10 mm/l
22
Q
hypovolemic hyponatremia treatment
A
isotonic saline
23
Q
what is euvolemic hyponatremia
A
elevated total body water with a normal total body sodium
24
Q
causes of euvolemic hyponatremia
A
glucocorticoid deficiency, hypothyroidism, pain, psych, drugs, SIADH
25
urinary sodium concentration in euvolemic hyponatremia
>20 mmol/l
26
euvolemic hyponatremia treatment
fluid restriction
27
what is hypervolemic hyponatremia
greatly elevated total body water and elevated total body sodium
28
causes of hypervolemic hyponatremia
nephrotic syndrome, heart failure, cirrhosis, acute/chronic renal failure
29
urinary sodium concentration in hypervolemic hyponatremia
acute/chronic renal failure: >20 mmol/l. all other causes: <10 mmol/l
30
hypervolemic hyponatremia treatment
fluid and sodium restriction
31
where is dietary potassium absorbed
intestines
32
where is potassium excreted
distal tubule
33
what facilitates intracellular uptake of potassium
insulin
34
hormonal consequences of hyperkalemia
stimulates secretion of aldosterone
35
causes of hypokalemia
loop diuretics, albuterol, vomiting, diarrhea, hyperinsulinemia
36
ssx of hypokalemia
muscle weakness, arrhythmias
37
ECG changes in hypokalemia
u waves, flattened T-waves
38
causes of hyperkalemia
CKD, hyperglycemia, hyperosmolality (why?) insulin (why?), beta blockers (?), rhabdo
39
ssx of hyperkalemia
muscle weakness, paralysis, arrhythmias, bradycardia
40
ECG changes in hyperkalemia
peaked T-waves, widened QRS
41
name of grading system for ulcers
Wagner
42
Wagner grade 2 ulcer
involves ligament, tendon, joint capsule, or fascia without abscess or osteomyelitis
43
Wagner grade 3 ulcer
deep ulcer with abscess or osteomyelitis
44
Wagner grade 4 ulcer
gangrene to forefoot
45
Wagner grade 5 ulcer
extensive gangrene
46
Wells criteria high risk
greater than or equal to 3
47
Wells criteria moderate risk
1-2
48
Wells criteria low risk
less than 1
49
Wells criteria components
active cancer, stasis, bedridden due to surgery, deep vein tenderness, entire leg swollen, unilateral calf swelling/pitting edema, prior history of DVT/PE
50
edema type: predilection for medial ankle/calf
venous insufficiency
51
edema type: tender with positive Homans sign
DVT
52
edema type: early pitting, late fibrotic/hyperkeratotic
lymphedema
53
edema type: nonpitting, affecting legs but sparing ankles and feet
lipedema
54
edema type: associated with weeping ulcerations over medial malleolus
venous insufficiency
55
edema type: associated with hemosiderin deposition
venous insufficiency
56
edema type: Inability to tent skin over second digit
lymphedema
57
edema type: warmth over affected extremity
DVT or cellulitis
58
edema type: associated with lipodermatosclerosis
venous insufficiency
59
edema type: nonpitting, generalized, periorbital, yellow-orange skin discoloration over knees, elbows, palms, soles
myxedema
60
Kaposi-Stemmer sign
inability to tent skin over second digit
61
edema type: prominent malleolar fat pads
lipedema
62
May-Thurner syndrome
compression of the left iliac vein by the right iliac artery in young women causing edema of the LLE
63
likely etiology of edema in obstructive sleep apnea
pulmonary hypertension (does not explain all cases)
64
treatment for mild venous insufficiency
compression stockings at 20-30 mmHg
65
treatment for moderate-severe venous insufficiency
compression stockings at 30-40 mmHg
66
compression stocking contraindication
PAD (must be careful because venous insufficiency may coexist with PAD)
67
how to assess for PAD
ankle-brachial index
68
edema type: associated with stasis dermatitis
venous insufficiency
69
treatment for stasis dermatitis
topical steroids and emollients
70
treatment for lymphedema
manual lymphatic massage, compression at 30-40 mmHg, pneumatic compression devices
71
what is post-thrombotic syndrome
chronic leg swelling, cramping, pain, skin changes in those with prior DVT
72
how to prevent post-thrombotic syndrome
use compression stockings in addition to anticoagulants for DVT
73
what is factor V leiden
hypercoagulable state and increased thrombin generation caused by genetic defect leading to inability to break down factor V
74
how is factor V leiden diagnosed
activated protein C, genetic testing, others
75
what antibodies can be elevated in the case of thrombisis
antiphospholipid antibodies
76
protein C and S functions
work as part of natural anticoagulant system
77
causes of protein C and S deficiency
genetic, liver disease, warfarin, malnutrition, autoimmune disorders (S only), active clotting states (eg venous thrombosis)
78
what is antithrombin III
a globulin produced in liver that inhibits coagulation, provides most of the anticoagulant effect of heparin
79
causes of antithrombin III deficiency
genetic, liver disease, malignancy, DIC, acute thrombosis, nephrotic syndrome
80
at what percentage of occlusion do symptoms appear in PAD
70%
81
PAD pain in hips/buttocks
aorta or iliac artery involvement
82
PAD pain in thigh
iliac/common femoral artery involvement
83
PAD pain in upper 2/3 of calf
superficial femoral artery
84
PAD pain in lower 1/3 of calf
popliteal artery involvement
85
PAD pain in lateral calf (per Laura)
tibial artery involvement
86
pathophys of ischemic ulcers
start as small traumatic wounds and have insufficient blood supply for healing
87
ischemic ulcers location
pressure points, malleoli, toe joints, shin
88
ischemic ulcers presentation
dry, punched-out, painful, little bleeding
89
normal ABI range
1.0-1.4
90
borderline ABI range
0.91-0.99 (can proceed to exercise testing)
91
false negative ABI range
>1.4 (can proceed to toe brachial index)
92
severe PAD ABI range
<0.4
93
mild-moderate PAD ABI range
0.4-0.9
94
gold standard for PAD imaging
conventional arteriography
95
usual 1st-line advanced imaging for PAD
CT angiography
96
components of Virchow's triad
stasis, hypercoagulability, endothelial injury
97
what is best anticoagulant choice in elderly
DOACs (rivaroxaban, apaxiban)
98
advantages of DOACs
easy to monitor, short half-life
99
how much delay until onset of action for vit k antagonists and why
5 days because of half-life of previously formed coag factors
100
how long to continue heparin bridge
for 5 days after starting vit k antagonist and until INR is within target range for 24 hours
101
recommended duration of anticoagulation after first instance of VTE due to reversible risk factor
3 months
102
recommended during of anticoagulation after first instance of unprovoked VTE not attributable to reversible risk factor
lifelong if low or moderate bleeding risk, 3 months if high bleeding risk
103
when can a VTE not involve anticoagulation
if mild distal DVT without severe symptoms, may use serial monitor instead of anticoagulation for first two weeks
104
what should patients do after completion of anticoagulation course?
take aspirin lifelong
105
if VTE recurrence while on vit K antagonist or DOAC
switch to LMWH
106
when should INR be obtained when initiating vit k antagonist therapy
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
what to do if INR<4.5 but greater than goal
hold dosage and resume at a lower dose once INR is within therapeutic range
108
what to do if INR is 4.5-10
hold the next 1-2 doses, increase monitoring, resume at lower dose once INR is within range
109
what to do if INR is >10
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
timing of vit k antagonist dosage
should be taken at the same time every day
111
components of CHADS2
CHF, HTN, Age over 75, DM, prior Stroke
112
which DOAC confers higher risk of GI hemorrhage
rivaroxaban
113
elements of HAS-BLED
HTN, Abnormal renal function, Stroke, Bleeding, Labile INR, Elderly, Drugs/alcohol
114
DOAC half-life
approx 12 hours
115
Beta 1 selective drugs
metoprolol, atenolol, esmolol
116
key side effect of clonidine
rebound HTN
117
main effect of dihydropyridine CCBs
vasodilation
118
ACE I's and ARBs can cause what electrolyte disturbance
hyperkalemia
119
majority of PAD obstructions location
popliteal artery
120
beri beri
thiamine deficiency
121
main cause of lymphedema industrialized world
cancer
122
why does renal failure cause edema
fluid overload, protein loss via glomerulus, oversecretion of renin
123
edema type thin skin tight with water
protein malnutrition
124
medications causing edema
steroids, hormones, NSAIDs, CCBs (peeeeens)
125
"hormonal cascade of death"
obstructive sleep apnea
126
pitting edema grading scale
0-4
127
Leriche Syndrome
ED, aorto-iliac PAD, ass pain
128
drugs for PAD
statins, ASA, ACE-inhibitors, plavix, pletal (cilostazol)
129
congenital primary lymphedema
Milroy (born without lymph nodes)
130
primary lymphedema in females 1-35 y/o
lymphedema praecox (Meige disease)
131
what is horse chestnut seed extract for
venous insufficiency
132
what is peau dorange associated with
lipedema
133
what type of afib requires warfarin
valvular
134
goal INR for warfarin
2-3
135
muscle holds how much ICF
75%
136
what percent of ECF is in veins
85%
137
effective osmoles
Na, glucose
138
ineffective osmoles
alcohols, lipids, proteins
139
drug triggers for ADH release
NSAIDs, SSRIs, cancer drugs, seizure meds, tumors
140
pseudohyponatremia
some interfering factor causing a false hyponatremia (lipids, proteins, urea, immunoglobins)
141
severe hyponatremia cutoff
under 120
142
where is potassium excreted
distal tubule
143
thiazide diuretics side effects
hypokalemia, hyperlipidemia, hyperglycemia, hypercalcemia, hyperuremia
144
criteria for orthostatic hypotension
decrease of 20 mmHg systolic or 10 mmHg diastolic within 3 minutes of standing
145
thiazides mechanism of action
inhibit sodium reabsorption in distal convoluted tubule
146
what part of nephron do carbonic anhydrase inhibitors affect
proximal convoluted tubule
147
what must be monitored in patients taking loop diuretics
potassium and creatinine
148
effects of angiotensin II
vasoconstriction, aldosterone release, increases Na resorption, stimulates thirst, stimulates release of ADH
149
effects of aldosterone
increases Na resorption (slower than angiotensin II because it is a hormone)
150
when is pharmacologic intervention for HTN recommended
>10% 10 year risk and BP>130/80
151
electrolyte imbalance that can occur with ACEI
hyperkalemia
