Endocrine Flashcards

(131 cards)

1
Q

Dopamineprolactin

A

Dopamine inhibitsprolactin
Low dopamine= lactogenésis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Arterial supply pituitary

A

Superior and inferior hypophyseal arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Thyroid surgery nerve risk

A

Protect recurrent laryngeal nerve when lighting inferior thyroid a
Superior laryngeal - superior thyroid a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Congenital hypothyroidism

A

Course facial features, short stature, mental impairment
“Pot belly” protruding umbilicus
Puffy face, protruding tongue
Pale skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Thyroid peroxidase

A

Iodide → iodine
Adds to tyrosine residues on thyroglobulin
Combines MIT + dit or dit x2 to make t3 or t4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Thyroglobulin

A

Large protein, many tyrosines
Tyrosines → MIT, dit → t3/4
Found in follicular cell lumen
When ready endocytosed into cell and cleave d by proteases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

5’ deiodinase

A

At tissues
T4 → active t3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Wolff chaikoff effect

A

Excess iodide inhibits TPO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Thyroid binding globulin

A

Transports almost all t3 and t4 in blood
Inactive whenbound
Increased during pregnancy and with OCPs - bound elevated, free normal
Decreasedhepatic failure, steroids-bound low, free normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Thyrotoxic crisis

A

Thyroid storm
Triggered acute physiologic stressors
Agitation, delirium
Fever
Diarrhea
Tachyarrythmia - high output heart failure- A fib
Coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Antithyroid antibodies graves

A

Anti tsh-r

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Tx hyperthyroid

A

Propranolol for tachycardia
Antithyroid propylthiouracil or * methimazole - PTU in first tri preg
Prednisone for exophthalmos if present

If failed:
Radioactive ablation
Thyroidectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Irregularly enlarged thyroid

A

Multinodular goiter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Antibodies hashimotos

A

Anti-tpo, thyroglobulin, microsomal ig G

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hla hashimotos

A

DR 3/5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Atrophic thyroiditis

A

Blocking-anti.TSH-R
Absent goiter
Middle age to elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Drug induced hypothyroidism

A

Amiodarone- antiarrythmic
Lithium
Aspirin
Sulfonamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Myxedema coma

A

Diminished mental status
Low temp
Hypoglycemia
Hyponatremia
Hypoxia
Hypoventilation
Bradycardia
Hypercapnia

Often neither myxedema nor coma…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Calcitonin tumor marker

A

Medullary thyroid cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Thyroglobulin tumor marker

A

Papillary or follicular thyroid cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

CEA tumor marker

A

Carcinoembryoniz antigen
Medullary thyroid, colon, pancreas, lung, breast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Biopsy hashimotos

A

Lymphocytes and hurthle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Painful enlarged thyroid low thyroid

A

Subacute granulomatous / de quervain thyroiditis,
Usually precipitated by acute viral infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Thyroiditishyperthyroid

A

Silent lymphocytic - May also be asymptomatic - often self- limita and mild- may progress to mild hypothyroid
De quervain thyroiditis
Or transient in ear h ly disease course hashimotos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Riedel thyroiditis
Fibrosis due tochronic inflammation Low or euthyroid Painless goiter Local compressive sx
26
Methimazole
Preferredantithyroid drug except in pregnancy Inhibits iodine → tyrosine and iodotyrosine coupling
27
Propylthiouracil
2nd choiceantithyroid Preferred inpregnancy first tri Similar Mx to methimazole Plus 5' deiodlinase inhibition of t4→t3
28
Antithyroid Æs
Agranulocytosis Liver damage Anca - antineutrophö cytoplasmic ab Vasculitis with glomerular injury More common ptu
29
Thyroid adenomas
Generally benign Most nonfunctional, some secretory No tumor capsule invasion or blood vessel invasion
30
Papillarythyroid carcinoma
Most commonmalignancy of thyroid Great prognosis Likely t4 secretory
31
Papillary thyroid carcinoma mutations
Ret or braf Or childhood radiation
32
Oxytocin production
Mostly PVN of ht
33
Oxytocin storage
Posterior pituitary
34
Prolactin sex hormones
Reduces GnRH Thus _ low T and E Implicated in infertility
35
Sheehan syndrome
Postpartum hemmorhage- → pituitary infarction → low prolactin → lactation failure, menstrual irregularities
36
Thyroid andprolactin
TRH, - → TSH and prolactin Primary hyperthyroid eg graves or secondary hypothyroid → low prolactin
37
Pituitary stalk compression prolactin
Hyper prolactinemia Interrupts inhibitory dopamine signal
38
Hyper prolactin causes
Dopamine blockers eg. Antipsychotics Prolactinomas Pituitary stalk compression Pregnancy Primary hypothyroid dt TRH increase End stage renal disease unknown why
39
Estrogen prolactin
Directly increases
40
Progesterone prolactin
Inhibits milk production effects eg pregnancy
41
G H starvation
-increased t o stabilize blood sugar By ghrelin
42
Congenital gh deficiency
Poor linear growth after first few months Delayed motor muscle Devi
43
Laron syndrome
Similar to manifestations ofcongenital gh deficiency but gh not → IGF So high gh low IGF
44
Childhood gh deficiency
Short stature, doll-like or infantile facial features Check IGF levels ( more consistent than_gh), bone Age Ro causes of failure
45
Testinggigantism
Oral glucose boles would normally decrease gh but not in true gigantism Dd: marfan, precocious puberty, normal genes
46
Acromegaly
Adult high gh Joint pain, muscle aches, gradualoftenunnoticable while happening hand and foot growth c coarse facies Diabetes, atherosclerosis dt glucose and lipid fx Causes: - tumor - mccune Albright - men-1 - carney complex - x linked acrogigantism
47
Tx Gh excess
Octreotide - somatostatin analog
48
Somatostatin
Secreted by ht to decrease gh
49
Hyper prolactin Tx
Cabergoline Bromocriptine Note these ore also implicated in hypo when taken for other reasons eg. Pd Or removal - based on severity. of visual field defects
50
ACTH deficiency
Mild: postural hypotension and pots Severe: weight loss, fatigue, low libido, hypoglycemia Extra bad: fatal vascular collapse - shock
51
ADH deficiency
Central di High volume dilute urine Dehydration, thirst, dizziness
52
Pituitary apoplexy
Sudden pituitary hemorrhage Trauma, aneurysm Emergency Low ACTH → shock Sudden excruciating headache, diploma, progressive hypopituitarism Immediate tx: stabilize bp with fluids and cortisol Also Tx hypoglycemia
53
PTH
Increased blood calcium Low bone density Low phosphate -renal exchange Gut uptake, urine reuptake, vitamin D production i bone breakdown
54
Hyper calcemia sx
Asymptomatic at first Then: Fatigue Irritability Depression Memory problems Decreased bone density if dt high PTH Then: Shortened qt_interval Arrhythmia Fractures Kidney stones Acute pancreatitis Ulcers Ab pain, constipation Stupor, confusion Seizures, coma
55
Men1 and men 2 both cause
High PTH
56
Men- 1 Gene
Men 1
57
Men 2a Gene
Ret
58
High PTH sx
Hypercalcemia Pain Bones, kidney stones, ab groans, psych moans
59
Osteitis fibrosis cystica
High PTH → cystic bone lesions Brown color tumors dt hemorrhage → hemosiderin deposits Rank-l expression on osteoblasts, rank on osteoclasts
60
Secondary hyper PTH
Dt chronically * low calcium Most common CKD dt low vitamin D conversion to active form in renal tubules by 1-a-hydroxylase Other causes _ malabsorption, vitamin D deficiency
61
Primary hyperPTH tx
Bisphosphanates eg alendronate decrease bone loss Cinacalcet mimics ca to turn off PTH Surgery possible but often fails, tricky
62
Polyuria calcium
High Ca → polyuria via inhibition of action of ADH in renal tubules = nephrogenic di Also potentially type I renal tubular acidosis, AKI
63
Acute hypercalcemia
Most often dt cancer dt: - pthrp production - metastasis bone - ectopic1-a-hydroxylas e→ excess calcitrol vitamin D
64
Causes hypercalcemia
Parathyroid Cancer Granuloma- 1 alpha hydroxylse production Meds: -Lithium - thiazide diuretics - excess Ca or vit Dsupplement -Familial hypocalcuric hypercalcemia - defects in ca receptors inparathyroid and kidney
65
Calcium action potential
Blocks sodium channels Raises threshold Weakness
66
Calcium heart
ReCduced Na movement de Ca blocking channels Less depolarization → shorter depolarization Shortened q T interval Later arrhythmia, St changes Cv. calcium deposits → valve stenosis, HTN, cardiomyopathy
67
Loop diuretics ca
Decrease Loops lose ca Used in symptomatic hypercalcemia t x
68
Acute symptomatic hyper Ca Tx
#1 fluids 2. Loop diuretics 3. Bisphosphanates Calcitonin if severe but resistance if long term Cancer: denosumab anti-rank-l High pth: cinacalcet Granulomatous and lymphoma: prednisone
69
Resorption
Breakdown of bone
70
Pancreatitis calcium
Acute pancreatitis can cause low Ca dt deposits forming High Ca can cause pancreatitis - one of the "groans"
71
Drugs causing hypocalcemia
Loop diuretics eg furosemide Bisphosphonates Cinacalcet Foscarnet_antiviral
72
Loop diuretics target
Na-k-2cl transporter thick ascending loop of henle
73
Chvostek sign,
Hypocalcemia Tap facial nerve → twitching
74
Trousseausign
Hypocalcemia Inflate bp cuff 3 min → hand twitching and contracture
75
Severe hypocalcomia st
Laryngospasm Bronchospasm Seizures Life threatening
76
Hypocalcemia reflexes
Hyperreflexia
77
Hypocalcemia st
Irritability of nerves, muscles, heart M sk: Numb/tingle Twit ching Hyperreflexia Tetany PsyCch: Anxiety Depression Psychosis Am s .chronic: Parkinsonism , dementia, cataracts Heart Prolonged qt interval Torsdades de pointes- potentially fatal
78
Albumin Ca
Transports Standard Ca lab is total including albumin bound but only free is active Free isphysiollogically important So low albumin means total Ca will be low or normal even if free is normal or high
79
Acute symptomatic hypocalcemia Tx
Iv calcium gluconate then transition to oral Ca with vit D Underlying cause
80
Bisphosphonattes
Prevent bone resorption Lower serum Ca Induce apoptosis in osteoclasts - dronate AES: -N/v - esophageal erosions - iv: jaw osteonecrosis
81
Denosumab
Hyper - Ca of malignancy Prevents resorption Decreases serum Ca Anti-rank-l Blocks osteoclast maturation
82
Hypo-mg
Causes hypo-ca Reduces PTH release Poor diet, alcohol
83
Sevelamar
Gut phosphate binder For hyper. Phosphate → hypo-ca of CKD
84
Calcium acetate
- Gut phosphate binder Good if Ca supplement also needed but use caution in CKD
85
Zone glomerulosa adrenal
Outermost Mineralocorticoid'S
86
Zone fasciculat a
Middle layer of cortex Less staining due to high lipid content Glucocorticoids
87
Zone reticularis
Innermost oadvenal cortex Androgens
88
Chromaffin cells
Adrenal medulla Catecholamine'S
89
ACTH cellular targets
Upregulate StAR - steroidogenic acute regulatory protein - rate limiting incortisol formation - transferscholesterol into mitochondria StimulatesCholesterol desmolase - convertscholesterol to pregnenolone
90
CBG
Cortisol binding globulin Transports most of cortisol in blood, prolongs t 1/2
91
Cortisoltarget
Intracellular gr-glucocorticoid receptor Complex directly binds glucocorticoid response element of gene
92
Cortisol bone
Decreases osteoblast ' activity excess → less new bone generation i i weaker bones
93
Cortisol neutrophils
Demargination Artificially increases count but decreases function
94
Cushing disease
Cushing syndrome caused by an ACTH- secreting pituitary adenoma Syndrome: all cause
95
Bp cushings
Diastolic htn
96
Bilateraladrenal_hyperplasia_tx
Cortisol synthesis inhibitors Metyrapone Ketoconazale Mitotane
97
Hyperaldosterone acid base
Metabolic alkalosis- excess H+ loss
98
Conn syndrome
Benign aldosterone-secreting adenoma of adrenal gland
99
Hypokalemia EKG
T wave inversion Prominent U waves
100
Main test to distinguish primary from secondary hyper-aldosteronis m
Plasma renin Renin →aldosterone So elevated in secondary and low in primary
101
Hyper-aldosterone Tx
Underlying cause K sparing diuretics - spironolactone and eplerenone
102
Spironolactore
Competitive aldosterone receptor antagonist Cortical collecting duct K sparing diuretic AES - androgen t progesterone - gynecomastia
103
Eplerenone
More specific aldosterone receptor antagonist K sparing diuretic Alternative to spironolactone No gynecomastia
104
Causes of secondary hyperaldosteronism
Renal artery stenosis - impaired read blood flow J G cell tumors Liver cirrhosis Hear t failure Nephrotic syndrome
105
Usually first presenting sign hyper aldosterone
Refractory hypertension Labs then show hypokalemia and metabolic alkalosis
106
Congenital adrenal hyperplasia
Autosomal recessive Usually low cortisol and aldosterone but high sex steroids Generally masculinizing - external genital ambiguity in female
107
Most commonenzyme deficient cah
21 -hydroxylase
108
Classic vs. nonclassic CAH
Classic - salt-wasting, dehydration, adrenal crisis - most common. Non-classic- non-salt wasting - partial enzyme fx makes aldosterone but still no cortisol → less severe → may be silent till puberty → generally nogenital ambiguity but will have precocious virilizing puberty Simple virilizing -cortisol andaldosterone present but high DHEA i
109
Pheochromocytoma MEN
Types 2a and 2b
110
Neuroblastoma
Abdominaltumor arising from neuralcrest cells Generally along sympathetic chain or in adrenal medulla Usually kids <4 Rapid growth Hypertension from renal artery compression or catecholamine secretion Rapid involuntary eye movements Muscle twitchin Abdominal distention Palpable mass
111
Neuroblastoma gene
Usually MYCN Amplification If present isassociated with more aggressive course with 50%mortality Without mutation better px with chance of spontaneous regression
112
Biopsy neuroblastoma
Homer-wright rosettes Small, round blue cells in circular patterns Eosinophilic neuropil IHC bombesin
113
Suppression testing pheochromocyta
ClonidineSuppression testing if 24 h urine catacholemine and metarephrines is indeterminate
114
Octreotide
Inhibits insulin and gh release Chronic hypoglycemia Acromegaly Esophageal bleed Hepatorenal syndrome
115
HLA T1DM
Dr3 and dr4
116
Hs type TIDM
. Type 4
117
Mechanism of microvascular damage in diabetes
Mostly non-enzymatic glycosylation of various cellular proteins. - ages In eye and Schwann cells - osmotic and oxidative injury from glucose → sorbitol
118
Rapid insulins
Lispro, aspart, glulisine
119
Intermediate acting insulin
NPH "
120
Long acting insulins
detemir, glargine
121
Metformin
Class: biguanide Mx: glut 4 phosphorylation → glucose uptake Also reduced gluconeogenesis and reduced gutreabsorption. Ae: lactic acidosis. Gi Ci: renal failure, CHF, hypoxia
122
-glitazone
Class: thiazolidinediones Mx: ppar- gamma activation → fatty acid storage → insulin sensitivity Ae: fluid retention, liver damage, weight gain, low bone density Ci: CHF
123
Gly-/gli-
Class: sulfonylureas Mx: stimulate pancreatic insulin release by closing atp-sensitive k channels Ae: hypoglycemia, weight gain Ci: sulfa allergy
124
_Glinide
Class: meglitinides Mx:similar tosulfornylureas Ok in sulfa allergy
125
- Gliflozin
Class: sglt-2 inhibitors Mx: inhibit renal glucose reabsorption Æ: UTI, dehydration, fatigue
126
Pramlintide
Class: amyline-anoloague Mx: slow gastric emptying, promote fullness Use: prevent hyper and hypoglycemia, weight loss, also T1DM
127
-Tide
Class; GLP -1 agonist Mx: endogenous incretin mimic - Increasedpostprandial insulin -Less glucagon - delayed gastric emptying -Fullness - weight loss Route: sub Q A E: gi upset, acute pancreatitis
128
_Gliptin
Class: Dpp4 inhibitor Mx: inhibits degradation of glp-1 Similar fx to glp-1 agonists Route: oral
129
Hormones inducing insulin release
Glp- 1 and GIP
130
Glucagonoma
Diabetes Depression Declining weight DVT Dermatitis - migratory necrolyticerethema
131
Vip-oma
"Pancreatic cholera"