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Endocrine > Things I don't know: PathoPhys > Flashcards

Things I don't know: PathoPhys Flashcards

1
Q

What should you do before giving TH in SEVERE hypothyroidism?

A

replace corticosteroids

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2
Q

Sx of thyrotoxic crisis

A

SOB, tachycardia, afib, vomit, diarrhea, jaundice, lost lots of weight
hyperthyroid that DIDN’T TAKE THYROID MEDS

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3
Q

Tx of thyroid storm

A

TREAT NOW
life threatening issues first: intubation, diuresis, anti-seizure meds
then: thionamide, iodine (stops them from making thyroid), gluccocorticoids, bile acid binder, nutrition
get free T3 to guide therapy

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4
Q

Mechanisms of damage in high glucose

A
  1. polyol pathway: sorbitol
  2. AGE formation (advanced glycation end product): ROS production
  3. PKC activation
  4. increased hexosamines
  5. PARP (poly ADP ribose polymerase)
  6. epigenetic (methylation/demethylation)
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5
Q

Who is at an increased risk of diabetic nephropathy? Most sensitive test?

A

increased urine albumin excretion
if untreated leads to end stage renal disease
maintain normal UAE: no nephropathy

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6
Q

How does insulin Tx affect someone with increased GFR and UAE?

A

UAE: returns to normal in T1DM, and many in T2DM return to normal
GFR: may remain elevated in both

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7
Q

What almost always accompanies proteinuria?

A

increase in BP

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8
Q

How long does it take micro-albuminuria to develop in T1DM?

A

5-15 yrs

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9
Q

What increases likelihood of lower limb amputation in diabetic?

A

symptoms of peripheral neuropathy

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10
Q

positive symptoms of diabetic peripheral neuropathy

A

pain, paresthesia, dysesthesia, allodynia

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11
Q

negative symptoms of diabetic peripheral neuropathy

A

decrease sensation to temp., pain, touch, motor movement

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12
Q

clinical staging of diabetic nephropathy

A
  1. nonproliferative diabetic retinopathy (NPDR): asymptomatic
  2. preproliferative diabetic retinopathy: laser therapy can prevent vision loss
  3. proliferative diabetic retinopathy (PDR): major cause of vision loss
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13
Q

epsilon cell of pancreas

A

secrete ghrelin

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14
Q

gamma cell

A

PP cell

secretes pancreatic peptide

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15
Q

Fn3K

A

deglycation of RBC

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16
Q

What causes the islet damage in DM?

A

islet specific T cells

Ab: GAD, ICA, IAA, ZnT8

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17
Q

HLA DR2/DR2

A

protective against T1DM

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18
Q

DQ beta chain

A

neg: susceptible to T1DM
pos: protection from T1DM
can be in middle
DR4/DR4 overrides protection

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19
Q

DQ7

A

primary protection against T1DM

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20
Q

DQ8

A

primary susceptibility to T1DM

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21
Q

amylin

A

B cells of pancreas
decrease gastric emptying
decrease glucagon secretion
promotes satiety

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22
Q

GLP-1

A

increase insulin secretion

decrease glucagon and gastric emptying

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23
Q

What can cause mental status change in SIADH?

A

brain swells

can also cause seizures

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24
Q

What osmotic factors can stimulate ADH?

A

Na, mannitol, urea

NOT: glucose

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25
Q

What are the non-osmotic factors than stimulate ADH?

A 
hypotension, hypovolemia
N/V
hypoglycemia
renin-angiotensin
Pain, stress, emotion?
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26
Q

Factors that alter AQP2 levels

  1. increase
  2. decrease
A
  1. CHF, pregnancy, SIADH

2. DI, postobstructive polyuria, chronic renal failure

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27
Q

Normal serum Na

A

136-145 mEq/L

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28
Q

What is renal tubular Na reabsorption regulated by?

A
  1. SGLT
  2. ANP
  3. Renin-angiotensin-aldosterone
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29
Q

causes of hyponatremia

  1. hypovolemic
  2. hypervolemic
  3. euvolemic
A
  1. high urine output and Na excretion, increase ANP
  2. edema (nephrotic syndrome, CHF, cirrhosis), water intoxication
  3. ADH mediated water retention
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30
Q

clinical presentation of hyponatremia

  1. early
  2. later
  3. chronic
A
  1. N/V, headache
  2. seizure, coma, resp. arrest
  3. lethargy, confusion, muscle cramps, neuro impairment
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31
Q

causes of SIADH

A 
paraneoplastic
trauma
CVA
infection: pulmonary, brain, near
drugs: cancer, psych
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32
Q

Tx SIADH

A

FLUID RESTRICTION

demeclocycline, lithium, vaptans

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33
Q

hypernatremia Sx

A

thirst, lethargy, irritable, seizure, fever, oliguria

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34
Q

Causes of hypernatremia

A
  1. DI
  2. Na excess
  3. water depletion exceeding Na depletion: diarrhea, vomit, dehydration
  4. drugs: lithium, cyclophosphamide, cisplatin
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35
Q

DIDMOAD syndrome

A

familial
central DI
DM, nerve deafness, optic atrophy, bladder and ureter atonia

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36
Q

water deprivation test

  1. Uosm after vasopressin increases 50%
  2. less than 50%
A
  1. central DI

2. nephrogenic DI or psychogenic

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37
Q

familial hypocalciuric hypercalcemia

A 
AD inactivating mutation in CaSR
mildly increased serum Ca and PTH
asymptomatic
low urine Ca (unlike primary hyperparathyroidism)
Tx: no intervention
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38
Q

drugs that induce hypercalcemia

A

lithium

HCTZ

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39
Q

PTH independent hypercalcemia

A
  1. tumor: PTHrP or bone metastases
  2. granulomatous disease (TB, sarcoidosis, lymphoma): increase vit. D
  3. multiple myeloma
  4. hyperthyroidism, adrenal failure
  5. immobilization
  6. medications: Vit. D, Vit. A, milk-alkali syndrome
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40
Q

primary hyperparathyroidism work up

A
  1. Ca, albumin
  2. PTH
  3. 25-OH vit. D
  4. 24 hour urine Ca (to differentiate from FHH)
  5. imaging: thyroid US (localize), 99Tc-sestamibi scan (localize), DXA
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41
Q

criteria that indicates parathyroidectomy

A
  1. Ca above 1 mg/dL above UNL
  2. less than 50 yrs old
  3. osteoporosis
  4. renal insufficiency
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42
Q

nonsurgical Tx for hyperparathyroidism

A

hydrate
bisphosphonates
Vit. D maintenance
cinacalcet

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43
Q

if hypercalcemia is due to malignancy, what will PTH be

A

suppressed

breast and squamous cell CA most common

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44
Q

What causes hypercalcemia in malignancy?

A

PTHrP
bony metastasis
cytokines activating osteoclasts
multiple myeloma: destroys bone

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45
Q

how do granulomatous disease cause hypercalcemia

A

increase 1 alpha hydroxylase which increases Vit. D
increase Ca, PO4
decrease PTH

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46
Q

tx of acute hypercalcemia

A

FIRST: address volume status: saline if dehydrated
then:
1. saline diuresis and furosemide: blocks Na/K ATPase causing Ca secretion
2. calcitonin (3rd line)
3. bisphosphonates
4. glucocorticoids (in myeloma, granulomatous disease, Vit. D toxicity)
5. dialysis

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47
Q

Work up for secondary hyperparathyroidism

A

Sx most likely due to underlying disease not PTH
serum PTH, Ca (with albumin), P, creatinine, Vit. D
do NOT need 24 hour urine Ca
no image studies if Ca normal
Tx underlying disease

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48
Q

weird causes of hypocalcemia

A
  1. acute pancreatitis: free FA chelate Ca
  2. massive transfusion: citrate binds Ca
  3. tumor lysis syndrome or rhabdomyolysis: Pi released binds Ca
  4. meds: Pi, bisphosphonates
  5. hungry bone syndrome
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49
Q

Sx of hypocalcemia

A 
agitation
HYPERREFLEXIA
convulsions
HTN
long QT
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50
Q

Work up of hypocalcemia
what does low PTH indicate?
high PTH?

A

albumin, total Ca x 2, PTH
low PTH: Mg deficiency, phosphate excess, hypoparathyroid
high PTH: severe vitamin D deficiency, renal failure, PTH or Vit. D resistance

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51
Q

pseudohypoparathyroidism

A

mutation in Gs alpha subunit
PTH resistance
hypocalcemia, hyperphosphatemia, high PTH
short stature, round face, short 4th metacarpal, obesity, Albright’s hereditary osteodystrophy

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52
Q

acute hypocalcemia crisis Tx

A

ALWAYS correct MAGNESIUM if low

Ca gluconate

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53
Q

long term hypocalcemia Tx

A
  1. Ca
  2. Vit. D (need active form unless PTH is present)
  3. Hydrochlorothiazide: increase renal reabsorption of Ca in distal tubule
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54
Q

hyperglycemic crises pathogenesis

A

insulin deficiency: increased glucose production, decreased glucose uptake
increases glucagon, GH, cortisol, catecholamines
hyperglycemia leading to osmotic diuresis leading to volume depletion

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55
Q

ketoacidosis

A

adipose: FA release
liver: increased ketogenesis
leads to ketoacidosis leading to decreased alkali reserve leading to metabolic acidosis
also get hyperglycemia leading to osmotic diuresis leading volume depletion

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56
Q

Dx of DKA

A 
plasma glucose greater than 250
LOW pH (less than 7.3)
LOW bicarb: less than 18
ketones: POSITIVE
Sx of drowsy only in moderate
Sx of stupor/coma: only in severe
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57
Q

Dx of HHS (hyperglycemic crises)

A 
pH greater than 7.3: NORMAL
bicarb greater than 18: NORMAL
anion gap is HIGH
serum osmol greater than 330
plasma glucose greater than 800
drowsy, stupor, coma
ketones: can be positive
58
Q

Causes of DKA and HHS

A

new DM
failure to take insulin
infection or medical illness

59
Q

presentation of DKA

A

polydipsia, polyuria, weak, hypothermia, tachycardia, altered sensorium
unique: WEIGHT LOSS, abdominal pain, ILEUS, N/V, tachypnea, KUSSMAUL breathing, ACETONE breath
SHORT ONSET

60
Q

presentation of HHS

A

polydipsia, polyuria, weak, hypothermia, tachycardia, altered sensorium
unique: Sx of accompanying illness, poor appetite, MENTAL STATUS CHANGE, HYPOTENSION
LONG ONSET

61
Q

lab studies for HHS and DKA

A

immediate: blood glucose and serum ketones
also: ABG, CBC, CMP, ketones, urinalysis
CMP: glucose, electrolytes, bicarbonate, PO4, Mg, BUN, creatinine

62
Q

anion gap

A

AG = Na - (Cl + HCO3)

63
Q

serum osmolarity

A

2Na + glucose/18 + BUN/2.8

64
Q

Tx in

  1. DKA
  2. HHS
A

DKA: lots of INSULIN (titrated to avoid hypoglycemia), normal saline, then hypotonic
2. some insulin, LOTS of fluid: normal saline, then hypotonic
do NOT give insulin until K is corrected

65
Q

corrected Na

A

(1.6 x glucose -100)/ 100

66
Q

DKA serum

  1. Na
  2. K
A
  1. hyponatremia

2. hyperkalemia

67
Q

markers for bone formation

A

ALP
osteocalcin
carboxyterminal propeptide of type 1 collagen (P1NP)

68
Q

markers for bone resorption

A

N-telopeptide

carboxyterminal of type 1 collagen (CTX-1)

69
Q

DXA

A

gold standard to measure bone mineral density (important predictor of fractures)

70
Q

clinical evaluation of osteoporosis

A

Ca, PO4, inactive (25) Vit. D, DXA

71
Q

T score of osteoporosis Dx

A

less than -2.5

or LOW TRAUMA fracture and greater than -2.5

72
Q

meds that increase fracture risk

A

glucocorticoids, TCA, benzodiazepines, antipsychotics, PPIs, SSRIs, anticonvulsants, aromatase inhibitors, androgen deprivation therapy

73
Q

fracture risks

A 
femoral neck T score
age
previous low trauma fracture 
low BMI
smoking
steroids
RA
High alcohol use
family Hx
74
Q

endocrine mediated causes of low bone mass density

A 
cushing's
hypercalcemia, kidney stones
acromegaly
hypogonadism
hyperthyroidism
75
Q

Tx of osteoprosis

A

stop smoking/drinking
increase exercise
Ca, Vit. D
fall prevention

76
Q

Osteoporosis: who do you give meds

A
  1. T score less than -2.5 after age 50
  2. osteopenia with Hx of fragility fracture
  3. use FRAX score for under 50 and T score less than -2.5 or older than 50 with greater than -2.5
77
Q

inherited Ricket’s

A

AR
low Vit. D: 1 alpha hydroxyls deficiency
high Vit. D: receptor defect

78
Q

Bone pain

A

fibrous dysplasia
osteitis fibrosa cystica
osteogenesis imperfecta
Paget’s

79
Q

McCune-Albright

A 
GNAS1 gene mutation
precocious puberty
fibrous dysplasia
cafe au lait
hypophosphatemia due to FGF-23
80
Q

corrected Ca (when albumin is low)

A

(0.8 x (4 - patient’s albumin) + serum Ca

81
Q

most common cause of acromegaly

A

pituitary MACROadenoma

82
Q

What are GH levels after oGTT?
normal
acromegaly

A

normal: less than 1 ng/ml
acro: greater than 2 ng/ml

83
Q

acromegaly Sx

A 
large hands, feet
maxillofacial change
arthralgia
excess sweating
headache
hypogonadal
sleep apnea
HTN
DM
84
Q

Prolactin levels

  1. normal
  2. prolactinoma
  3. macroprolactinoma
A
  1. lower than 25 ug/l
  2. greater than 250
  3. greater than 500
85
Q

drugs that cause high prolactin

A

antipsychotics: DA antagonist

reserpine, haloperidol

86
Q

labs for TSH secreting pituitary adenoma

A

RARE
high T4 and TSH
confirm with MRI

87
Q

What should you give to a patient that has central (pituitary) hypothyroidism along with levothyroxine?
why?

A

glucocorticoids
TH replacement therapy causes accelerated metabolism of endogenous cortisol causing adrenal insufficiency
need to evaluate adrenal reserve

88
Q

commonly one of the first derangements of cushings

A

failure to achieve normal late night (11pm to 1am low cortisol) circadian nadir

89
Q

Dx of cushing

A
  1. 24 hour urine free cortisol
  2. late night salivary cortisol
  3. 1 mg overnight dexamethaonse suppression test (give 1 mg at 11pm-12am and measure at 8am)
  4. longer low dose DST (2 day, 2 mg dose every 6 hours for 8 doses; check 2 or 6 hours after last dose)
90
Q

Who gets false positives for overnight dexamethasone suppression test?
why?

A

women on oral contraceptives

increase CBG, but measure total cortisol rather than free

91
Q

what should cortisol be in dexamethasone suppression test

A

normal: less than 1.8 mug/dl

92
Q

what should you suspect in a patient with acute unexplained volume depletion and shock

A

acute adrenal insufficiency

hyperkalemia, acidosis, hypoglycemia

93
Q

Dx of adrenal insufficiency

A

ACTH stimulation test

94
Q

mutation in CYP21A2 gene

A

21-hydroxylase deficiency

can’t convert 17-hydroxyprogesterone to 11-deoxycortisol

95
Q

congenital adrenal hyperplasia: 21-hydroxylase deficiency: girl presentation

A

salt losing and non-salt losing
NEONATE presentation
ambiguous genitalia, clitoral enlargement, common urethral-vaginal orifice, partial or complete fusion of labia
NORMAL internal female organs, salt losing crisis

96
Q

congenital adrenal hyperplasia: 21-hydroxylase deficiency: boy presentation

A

salt losing crisis as infant
or toddler with signs of puberty (non-salt losing)
newborns may not show signs of CAH: sometimes scrotal hyper pigmentation, phallic enlargement

97
Q

salt losing crisis

A

hyponatremia
hyperkalemia
failure to thrive

98
Q

Dx of 21-hydroxylase deficiency

A

elevated 17-hydrocyprogesterone

greater than 3500 ng/dL

99
Q

nonclassical congenital adrenal hyperplasia

A

reduced 21-hydroxylase function
normal glucocorticoid and mineralocorticoid production
EXCESSIVE androgen production
NO salt wasting
Female does NOT have ambiguous genitalia
Sx in late childhood: premature puberty, acne, accelerated bone age
girls: hirsutism, irregular menstruation
boys: normal testicle function, some have infertility

100
Q

Dx of non classic congenital adrenal hyperplasia

A

suggested by: 17-hydroxyprogesterone greater than 200 ng/dl

confirmed with ACTH stimulation test: gold standard: 17-hydroxyprogesterone exceeding 1500 ng/dl

101
Q

primary hyperaldosteronism Sx

A 
HTN, hypokalemia, alkalosis, mild/NO hypernatremia (Na regulated by ADH), hypomagnesemia, muscle weakness, CV risks
NO edema (ANP limits Na retention)
102
Q

Dx of primary hyperaldosteronism

A

screen: plasma K
SIMULTANEOUSLY aldosterone: renin ratio greater than 30: specific and sensitive
aldosterone suppression: 2 L normal saline over 4 hrs with pt supine: normal aldosterone: less than 5 ng/dl

103
Q

Tx of primary aldosteronism

  1. solitary adrenal adenoma
  2. bilateral hyperplasia
A
  1. Sx to remove adrenal gland

2. spironolactone, eplerenone

104
Q

endocrine conditions associated with HTN

A

pheochromocytoma, mineralocorticoid excess, glucocorticoid excess
also: acromegaly, DM, obesity, CAH, estrogen induced, pregnancy induced, renin secreting tumors, hypo/hyperthyroid, liddle syndrome

105
Q

metabolic and vascular manifestations of pheochromocytomas

A

weight loss, hyperglycemia

plasma volume contraction: orthostatic hypotension, elevated hematocrit

106
Q

Dx of pheochromocytoma

A

urine: metanephrines, catecholamines
NE: 280 (normal 15-80)
Epi: can be normal

107
Q

pheochromocytoma Tx

A

pre-op: alpha and beta blockade, fluid
Sx
post-op: fluids, pressors

108
Q

regulation of aldosterone

A

volume of ECF

109
Q

syndrome of apparent mineralocorticoid excess

A

defects or drug/LICORICE inhibition of 11-B-hydroxysteroid dehydrogenase
allows normal cortisol levels to activate aldosterone receptors

110
Q

Cause of hypoglycemia
non-diabetic?
diabetic?

A

non: RARE: insulinoma, post-GI Sx, tumor, adrenal insufficiency, severe illness (hepatic, renal failure, sepsis), drugs
DM: almost always IATROGENIC

111
Q

alert value for diabetic at risk for hypoglycemia

A

blood glucose 70 mg/dL (3.9 mmol/L) or less

112
Q

severe hypoglycemia in DM

A

req. assistance of another to take corrective action

INCREASES MORTALITY

113
Q

documented symptomatic hypoglycemia in DM

A

symptoms and low BG (less than 70)

114
Q

asymptomatic hypoglycemia

A

no symptoms

low BG

115
Q

probable symptomatic hypoglycemia

A

symptoms

didn’t take a BG, presume low

116
Q

pseudo-hypoglycemia

A

symptoms

normal BG

117
Q

Sx of hypoglycemia

A

sweat, palpitations, hunger, nervous, dizzy, impaired concentration, blurred vision, tingling
severe: coma, death

118
Q

how does hypoglycemia cause death?

A

PROLONGED QT (K, Herg channels)
proinflammatory: ICAM, VCAM, E-selectin, VEGF, IL-6
increase platelet activation
decrease fibrinolytic balance (increase PAI-1)

119
Q

syndrome of hypoglycemia associated autonomic failure (HAAF)

A

reccurent hypoglycemia
hypoglycemia unawareness
defective counter regulation
must re-evalute regimen

120
Q

how many episodes of hypoglycemia does it take to blunt epinephrine response to hypoglycemia?

A

ONE

other counter regulators: cortisol, glucagon, GH

121
Q

Whipple’s triad

A
  1. sx/signs of hypoglycemia
  2. low plasma glucose
  3. resolution of Sx when glucose concentration is raised
122
Q

BMI

  1. underweight
  2. normal
  3. overweight
  4. obese class I
  5. class II
  6. class III
A

1.

123
Q

monogenic causes of obesity

A

RARE

  1. leptin def. or receptor def.
  2. melanocortin-4 receptor, POMC mutations
  3. PPARy2
  4. prohormone convertase-1 mutations
  5. TH receptor B mutations
124
Q

orexigenic agents

A

promote weight gain

  1. Neuropeptide Y
  2. melanin-concentrating hormone
  3. agouti-related peptide
  4. Ghrelin
  5. opioids
  6. endocannabinoids
    other: galanin, orexin, dynorphin, B-endorphin, NE/Epi, GHRH, Somatostatin, androgen, progesterone
125
Q

anerexogenic agents

A

promote weight loss

  1. leptin
  2. peptide YY
  3. alpha melanocyte stimulating hormone
  4. GLP-1
  5. serotonin
  6. cocaine, amphetamines
    other: insulin, ciliary neurotrophic factor, urocortin, neurotensin, CRH, bombesin, Cholecystokinin, enterostatin, DA
126
Q

opioids

A

weight gain

127
Q

endocannabinoids

A

weight gain
activated by: pain, anxiety
actions: induce appetiete, extinguish aversive memories, inhibit motor behavior, modulate temperature, hormone release and sm. muscle tone
receptors: CB1/2

128
Q

serotonin

A

weight loss

129
Q

ghrelin

A

weight gain

130
Q

glucagon-like peptide- 1

A

weight loss

131
Q

alpha melanocyte stimulating hormone (MSH)

A

weight loss

binds MC4R and reduces orexigenic effectors

132
Q

melanin concentrating hormone

A

weight gain

133
Q

agouti related peptide (AgRP)

A

weight gain

134
Q

neuropeptide Y (NPY)

A

weight gain

135
Q

peptide YY

A

weight loss

136
Q

cocaine-amphetamine regulated peptide (CART)

A

weight loss

137
Q

leptin

A

weight loss
made by adipose
inhibits: agouti-related peptide, neuropeptide Y
stimulates: POMC to produce MSH

138
Q

POMC

A

weight loss

139
Q

obesity Tx

  1. BMI over 35
  2. 30-35
  3. 25-30
A
  1. Sx
  2. drugs
  3. diet/exercise
140
Q

disease associated with obesity

A
  1. HTN: vascular sm. muscle hypertrophy, increase sympathetic tone: vasoconstriction, increase CO
  2. CAD: atherosclerosis (increase LDL)
  3. gallstones: increase turnover/excretion of cholesterol
  4. CA: estrogen, dietary carcinogens, cholesterol turnover increased
  5. HF: increase CO
  6. DM: insulin resistance
  7. sleep apnea
  8. decreased fertility
  9. psychosocial
141
Q

polyglandular autoimmune syndrome

A

autoimmune destruction of several endocrine glands
humoral and cell mediated immune mechanisms
ex: adrenal insufficiency and hypothyroidism

Endocrine (7 decks)

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