Extra Endocrine Flashcards
(191 cards)
1
Q
3 classic symtoms of prlactinoma
A
Galactorrhea, amenorrhea (females)
Impotence (males)
2
Q
why does prolactinoma cause amenorreha
A
Prolactin inhibits GnRH
3
Q
Secondary complication of growth cella denoma (besides growth) and its mechanism
A
Diabetes Mellitus, because growth hormone is gluconeogenic
4
Q
Diagnostic test for GH adenoma
A
Failure of glucose to suppress GH
5
Q
bone condition seen in women with prolactinoma and its mechanism
A
Osteoporosis
Prolactin inhibits GnRH = no estrogen = increased osteoclast activity
6
Q
Defect in dwarfism
A
Defective GH receptors
Elevated GH and low IGF-1 in serum
7
Q
what endocrine disease can cause a prolactinoma
A
Primary Hypothyroid
TSH backs up, TRH backs up, TRH stimulates Prolactin release
8
Q
Woman gives birth, begins breast feeding and then a week later she notices loss of pubic hair and difficulty with breast feeding
A
Sheehan syndrome
9
Q
Sheenan syndrome pathogenesis
A
During pregnancy, pituitary swells 2x but doesnt increase blood flow. If blood is lost during labor, pituitary infarcts
10
Q
Empty sella syndrome defect
A
Herniation of arachnoid and CSF into the sella, destroying the pituitary
11
Q
Sudden onset severe headache and bitemporal hemianopsia and diplopia
A
Pituitary apoplexy
12
Q
Major risk that central DI patients have
A
life threating dehydration
13
Q
Herediatry cause of nephrogenic DI
A
Mutation in neurophysin gene
14
Q
2 drugs that cause neprhogenic DI
A
Lithium
Demococlyine
15
Q
Most common site of ectopic ADH production
A
Small Cell Lung Cacner
16
Q
2 lab values that distinguish SIADH from DI
A
Sodium and serum osmolality
SIADH is hyponatremic, low osmolality, the others are hypernatremic, high osmolality
17
Q
Midline anterior neck mass in a child
A
Thyroglossal duct cyst
18
Q
how to differentiate thyroglossal duct cyst from branchial cleft cyst
A
Thyroglossal duct cysts move with tongue and while swallowing.
Brachial cleft cysts dont move and are on the lateral neck
19
Q
Child with mass at the base of the tongue
A
Lingual thyroid
20
Q
What is lingual thyroid composed of
A
Normal thyroid tissue
21
Q
2 receptors that mediate symptoms of hyperthyroidism
A
NaK pump –> increased BMR
B1 receptors –> increased SNS activity
22
Q
3 endocrine changes with hyperthyroid
A
Hypercalcemia (increased bone resorption)
Hyperglycemia (increased gluconeogenesis/glycogenolysis)
Hypocholesterolemia
23
Q
Graves disease defect
A
IgG stimulates TSH receptor
24
Q
3 PE findings of Graves
A
Goiter
Exopthalmos
Myxedema
25
Mechanism of GOiter in graves
Constant TSH = thyroid hyperplasia
26
mechanism of exopthalmos and pretibial myxedema
T cells stimulate Fibroblasts release to glycosaminoglycans --> increases osmotic swelling and adipocyte size --> exopthalmos
27
2 major cell types involved in exopthalmos
Fibroblasts
| T cells
28
2 specific glycosaminoglycans
Chondroitin sulfate
| Hyaluronic acid
29
Histology of graves
Tall follicular cells with colloid scalloping
Scalloped colloid looks like little tombstones --> like...GRAVES
30
Thiomide MOA
Blocks thyroid peroxidase
31
Patient with hyperthyroidism undergoes a surgery under general anesthesia. When they wake up they develop severe hyperthermia, Delerium, tachycardia and arrhythmias
Thyroid Storm
32
Toxic multinodular goiter defect
Nodules secreating hormone independent of TSH
33
Are hot nodules benign or malignant
Benign
34
Jod Basedow phenomenon
Patient with iodide deficiency is pumped full of iodide, and then they have thyrotoxicosis
opposite of wolff chaikoff
35
Infant with pot bellly, swollen face, protruding umbilicul, tongue falling out of mouth
Cretinism --> congential hypothyroid
36
6 Ps of cretinism
```
Pot belly
Protruding umbilicus
Protouding tongue
Pale
Puffy Face
Poor brain development
```
37
Dyshormonogenetic goiter defect
It is one of the causes of cretinsm.
Due to low levels of thryoid peroxidase
38
Myxedema cause
accumulation of glycosaminoglycans in skin and soft tissue
39
Patent states they've been gaining weight despite not eating more, feels fatigued and has noticed deepening of voice and feels like their tongue is larger than normal
Hypothryoidism
40
Why do hypothryoid patients have deeper voices/large tongues
Glycosaminoglycan deposition
41
Hashimoto defect (3 Ab)
IgG ab against thryoid peroxidase
IgG against thyroglobulin
Antimicrosomal Ab
42
HLA association with hashimoto
HLA DR5
43
classic paradox in lab findings in hashimoto
Patients initially present with elevated T4 levels and SSx of hyperthyroid, then come back and have SSx of hypothyroid
44
Why do T4 levels initially increase in hashimoto
follicle damage causes release of T4
45
2 unique histology findings of hashimoto
1- Germinal center formation (appears like a lymph node)
2- hurthle cells
46
hurthle cell description
Eosinophlic metaplasia that lines the follicles
47
which cancer does hashimotos increase risk for? why?
Diffuse large B cell lymphoma b/c germinal cells are being formed
48
Patient has an upper respiratory infection, then develops periodic episodes of tachycardia, sweating, increased appetite. C/o Jaw pain and anterior neck pain.
Subacute granulomatous Thyroiditis
49
Subacute granulomatous thyroiditis labs
Elevated ESR
50
SGT clinical course
Hyperthyroidism that may progress to hypothyroid
51
SGT biopsy
Granulomatous inflammation w/ giant cells
52
20 year old presents with dysphagia and wheezing. Thyroid is firm when palpated but not painful, and it doesnt move when palpated.
Riedel fibrosing thyroiditis
53
What must be r/o in fibrosing thyroitis? how?
Anaplastic thyroid cancer.
RF is in young patients, cancer is older. RF lacks malignant cells
54
how does I 131 uptake help distinguish hyperthyroid/toxic goiter from cacner
Cancer is a cold nodule (doesn't take up I 131)
55
5 classic cancers of the thyroid
```
Follicular Adenoma
Follicular Carcinoma
Papillary carcinoma
Medullary carcinoma
Anaplastic carcinoma
```
56
Hallmark of follicular adenoma on gross exam/histology
Follicles are surrounded by a thick fibrous capsule
57
CLassic risk factor for developing papillary carcinoma of thyroid
Radition to the head and neck area as a child
58
Papillary carcinoma histology (2 unique features)
Empty nuclei with central clearing (orphan annie cells)
Psammoma bodies
Papillary = Psammoma and Pupils (eyes)
59
Pap. Carcinoma spread and progonisis
Cervical llymph nodes
| Good prognosis
60
Follicular carcinoma mutation
RAS
61
Follicular carcinoma spread and prognosis
HEMATOGENOUS SPREAD. it forgot its a carcinoma
Good prognosis
62
Why can't fine needle aspiration differentiate b/w follicular adenoma and carcinoma
FNA only sample cells and not the capsule.
Entire capsule needs to be visualized under microscope to ensure no invasion
63
Medullary carinoma is a malignancy of
Calcitonin secreting parafollicular C cells
64
medullary carcinoma labs
Hypocalcemia w/ hypercalciuria (b/c calcitonin increases renal excretion of Ca)
65
Classic medullary carcinoma histology
sheets of cells in an amyloid (pink) stroma
66
Medullary carcinoma mutation
RET mutation (MEN2a 2b)
67
What should be done if pt has RET mutation?
Prophylactic thyroidectomy
68
What is the amyloid made of in med. carcinoma?
Calcitonin deposition
69
70yo pt presents with neck mass, dysphagia, hoarseness
Anaplastic carcinoma
70
Patient presents with asymptomatic hypercalcemia
Primary hyperparathyroidism
71
classic GI symptom that arrises in primary hyperPTH patients
Acute pancreatitis --> Ca is an enzyme activator!
72
4 main symptoms of hypercalcemia
"Stones, bones, groan, psychiatric overtones"
Kidney stones
Osteitis fibrosis cystica
Constipation, abdominal pain, pancreatitis
Depression
73
serum alk phos level in primary hyperPTH. Why?
Elevated b/c PTH activates osteoblasts, which secrete alk phos b/c it needs an alkaline environment to make bone
74
Osteitis fibrosa cystica cause
excessive bone resorption by overactive osteoclasts
75
OFC gross and Xray appearance
Cysts full of brown fibrous tissue
Multiple cystic spaces on Xray
76
Why is the cyst brown?
Hemosiderin form macrophages
77
2 most common causes of secondary hyperPTH
chronic renal failure
Hypovitaminosis D
Really, anything that causes low Ca or high Phos
78
Muscle effects of hypocalcemia
Muscle spasms and fatigue
79
2 PE findings for hypocalcemia
```
Chovestek sign (tap on facial nerve = twitch)
Trousseau (occlude brachail artery = carpal spasm)
```
80
3 most common causes of hypoparathyroid
Surgical excision of thyroid
Autimmune
DiGeorge!
81
spatial relationship of alpha and beta cells
Alpha cells surround the beta cells
82
hypersensitivity type of DM type 1
Type 4 --> T cells against beta cells
83
DM 1 histology vs DM 2
DM1 = inflammatory cells in the islet
DM2= Amyloid deposition in islet
84
Polyuria, polydipsia and glycosuria are due to
Hyperglycemia causing osmotic diuresis
85
WEight loss, decreased muscle mass and polyphagia are due to
Unopposed GLUCAGON. --> Does everything opposite of insulin
Increases lipolysis, protein breakdown, gluconeogenesis (which worsens the hyperglycemic symptoms)
86
SSx of DKA
DKA is Deadly
Delerium
Kusmaull respiration
Abdominal pain (N/V)
Dehydration
+ Fruity breath
87
why does DKA occur during illness?
Epinephrine is released --> epi causes glucagon release --> overactive lipolysis, glycogenolysis and gluconeogenesis
88
Mechanism for ketone body generation (3 steps)
Increaesd liposlysis --> increase FFA production --> liver converts FFAs to ketone bodies
89
2 reasons for hyperkalemia in DKA
No insulin = transcellular shift out of cells
| AG Metabolic Acidosis = transcellular shift out of cells
90
TOTAL body K levels in DKA
Decreased, even though theyre hyperkalemic (all the K is in the blood. none is in the cells)
91
3 Tx for DKA
Insulin (treat hyperK and lower glucose)
K+ so they dont become hypokalemic
Glucose so they dont become hypoglycemic
92
Why is DKA not seen in DM2?
Endogenous insulin prevents excess lipolysis (less FFAs = less ketone bodies)
93
how does obesity lead to DM 2
Adipose down regulates insulin receptors on cells
94
Stronger genetic predisposition b/w DM1 or DM2
DM2
95
HLA association in 1 and 2
DM1- HLA DR3 and DR4
| DM2- none
96
progression of serum insulin in DM2. Why?
INitially elevated due to hyperglycemia, but progressively decline as the beta cells burn out
97
3 diagnostic criteria for DM
Fasting BGL > 126
Random BGL >200
BGL > 200 2hrs after glucose load
98
hyperosmolar hyperglycemic non ketotic coma mechanism (3 steps)
Hyperglycemia --> osmotic diuresis --> dehydration
99
who is HHNS seen in ?
Elderly people who DONT DRINK WATER
100
HHNS ssx
Polyuria
Thirst
Lethargy
Seizures/neuro defecits
101
HHNS serum osmolarity, glucose and pH
```
Hyperglycemia
low osmolarity (water loss)
normal pH (no ketone bodies)
```
102
Non enzymatic Glycosylization causes which class of comlications
Small vessel disease (retinopathy, nephropathy, neuropathy)
| Large vessel disease (CAD, PVD, gangrene)
103
Osmotic damage causes which 4 complications
Peripheral neuropathy
Impotence
Blindness
Cataracts
104
3 cell types/tissues where osmotic damage occurs
Schwann cells
Pericytes of retinal blood vessels
Lens of the eye
105
Mechanism of osmotic damage
Accumulation of sorbitol in tissue = osmotic damage
106
2 enzymes responsible for osmotic damage
Elevated aldose reductase
| Decreased sorbitol dehydrogenase
107
DM can cause cataracts blindness and glaucoma. how are the mechanisms different?
```
Cataracts = osmotic damage to lens
Blindness = osmotic damage to pericytes
Glaucoma= non enzymatic glycoslylation of retina
```
108
Type of arteriolosclerosis seen in DM
Hyaline (just like HTN)
109
inheritance of MEN syndromes
Autosomal dominant. "MEN are Dominant"
110
MEN1 mutation
menin, a tumor supressor on Ch11
111
MEN1 SSx
Pituitary adenoma
Pancreatic tumor (ZE, gastrinoma, insulinoma)
Parathyroid adenoma
112
MEN2a SSx
Parathyroid adenoma
Pheochromocytoma
Medullary Carcinoma of thyroid
113
MEN2b SSx
Pheochromocytoma
Medullary carcinoma of thyroid
Mucosal neuromas
Marfanoid habitus
114
MEN2 defect and pathogenesis
RET mutation, which codes for receptor tyrosine kinase
115
embryonic origin of the cells affected by RET mutatino
Nueral Crest
116
SSx of Insulinoma
Episodic hypoglycemia and AMS that resolves with glucose administration
117
4 SSx of Somatostatinoma
Steatorrhea, gallstones (no CCK or secretin)
Glucose intolerance
Achlorhydria (n ogastrin)
118
VIPoma ssx (3)
Diarrhea (high VIP = relaxed bowel)
Hypokalemia (diarrhea...may also have NAGMA)
Achlorhydria (VIP inhibits gastrin)
119
Glucagonoma ssx (5)
```
Dermatitis
Diabetes
DVT
Declining weight
Depression
```
120
MCC of primary hyperaldosteronism
```
Bilateral adrenal hyperplasia
Adrenal adenoma (conn)
```
121
MCC of secondary hyperaldosteronism
Renal artery stenosis
CHF
ANything decreasing perfusion to the kidney
122
How to differentiate b/w primary and secondary hyperaldo
```
Primary = Low Renin w/o edema
Secondary = High Renin + Edema
```
123
Child with HTN, hypokalemia, elevated aldosterone with low renin
Glucocorticoid remediable aldosteronism (GRA)
124
GRA defect
Overactive expression of aldosterone synthase
125
confirmatory test for GRA
dexamethasone suppression
126
Liddle Syndrome defect
loss of ENAC channels = hyponatremia
127
how does Liddle and GRA presentation differ?
Liddle has low aldo and low renin
GRA has HIGH aldo and low rening
128
Mechanism of thin extremities in cushing
Cortisol causes proteolysis to get AAs for gluconeogenesis
129
Mechanism of obesity in cushing
High insulin and and glucose cause lipogenesis
130
Mechanism of striae in cushing
Cortisol inhibits fibroblast prolferation and collagen production
131
major eelectroloyte imbalance in cushing
Hypokalemia
132
Classic triad of symptoms that aren't related to physical appearance in cushings
HTN, hypokalemia and metabolic alkalosis
133
Mechanism for HTN inc ushings
cortisol increases catecholamine sensitivity in vessels --> vasoconstriction
Cortisol can increase Na reabsorption by acting like aldo
134
mechanism for hyhpokalemia/metabolic alkalosis in cushings
at very high doses, cortisol can actually bind to the aldosterone receptor (K and H secretion, Na reabsorption, HTN)
135
Basis for high dose dex suppression test
Pituitary cushings is suppressed with high dose dex
Ectopic cushings is not
136
Basis for CRH stimulation test in cushings
If ACTH increases when CRH is administered, it is pituitary cushings
If ACTH doesnt increase with CRH, it is ectopic production
137
imaging findings for exogenous steroid induced cushings
bilateral adrenal atrophy
138
2 causes of bilateral adrenal hypertrophy
Pituitary Cushings
| Ectopic Cushings
139
major cause of unilateral adrenal hypertrophy and atrophyy of the opposite gland
Adrenal adenoma
140
2 DDx for Hyperpigmentation of the skin in a person with adrenal dysfunction
Adrenal insufficiency
Congential adrenal hyperplasia
Anything causing low cortisol = high ACTH
141
major way to distinguish b/w 21OH and 11OH deficiency
21OH = hypotension , hyponatremia, hyperkalemia
11OH= Hypertension, hypernatremia, hypokalemia
142
21OH vs 17OH def (sexual appearance)
21OH is precocious puberty in males, ambiguous in females
17OH is amenorrhea in females and ambiguous in males
143
screening test of choice for any type of congential drenal hyperplasia
17-hydroxyprogesterone
144
17OHprogesterone screening results in each case
21OH- elevated
11OH - elevated
17OH- decreased
145
complication of over treating someone with cushings
they can develop adrenal insufficiency
146
why must corticosteroids must be tapered?
Acute withdrawal can lead to acute adrenal failure!
147
SSx of acute adrenal insufficiency
acute drop in BP to the point they can't perfuse organs
148
progressive onset of orthostatic hypotension, salt/sugar cravings, fatigue, weight loss
addison dz
149
2 MCC of addison disease
autoimmune destruction of the gland (DM)
| TB in developing countries
150
how to differentiate primary vs secondary adrenal insufficiency
Primary causes hyperpigmentation due to high ACTH
Secondary doesn't affect skin b/c ACTH is low
151
which cancer can cause adrenal insufficiency?
Lung cancer! remember, lung cancers met to the adrenals
152
Basis for metyropone stimulation test
Metyropone inhibits 11-deoxycortisol --> cortisol
Less cortisol should stimulate an increase in ACTH and 11-deoxycoritsol production
153
Metyropone test in primary ad. insuff.
ACTH increases, but 11-deoxycortisol does not
154
Metyropone test in secondary/tertiary ad. insuff
ACTH and 11deoxycortisol both remain low (b/c pituitary cant make more ACTH in response to the low cortisol)
155
Cell type and embryologic derivative of the adrenal medulla
Chromaffin cells
| derived from neural crest
156
Pheochromocytoma is a tumor of
chromaffin cells
157
Classic presentation of pheo.
EPISODIC
Anxiety/panic
palpitations
headaches
sweating
158
screening test for pheo
Vannilylmandelic acid (VMA) and catecholamines in the urine and serum
159
2 Tx for pheo, and the appropriate order
Phenoxybenzamine/phentolamine followed by Bblocker
160
2 Classic extra medullary site for pheochromocytoma
Inferior mesenteric artery
| Bladder wall
161
Neuroblastoma origin and location
chromaffin cells in kids
| neural crest origin
162
CLassic neuroblastoma presentation
abdominal distention
IRREGULAR shaped mass that CROSSES MIDLINE
HTN +/-
Myoclonus or Opsoclonus (eyes)
163
how to differentiate neuroblastoma from nephroblastoma (wilms)
Wilms is smooth and unilateral
164
Histology of neuroblastoma
Homer wright rosettes, just like medulloblastoma
165
Neuroblastoma gene defect
overexpression of N-myc
166
2 things that suppress GH secretion
Somatostatin
| GLucose
167
buzzword for the facial apperance of hyperthyroidism
"frightened appearance"
Refers to staring gaze with lid lag (eyes wide open)
168
mechanism of hypocholesterolemia in hyperthyroidism
Thyroid hormone increases LDL receptor synthesis in the liver --> decreases serum cholesterol
can increase risk of gallstones!!
169
effect of free T3/ rT3 in hypothyroidism
Can be low or normal
There is a lot of variability on the effects of T3 b/c it is made peripherally. So in early hypothyroid, T4 will be low, but the T3 can be normal because there isn't much of it around anyway. But in late disease, T3 will drop b/c T4 is severely low
170
Histology of orbital muscles in exopthalmos will show what 2 features?
Inflammation (T cells)
| Increased Adipocytes
171
4 Tx for thyroid storm
PTU
Prednisone
Propanolol
Potassium Iodine
172
LIgation of superior laryngeal artery during thyroidectomy. Complication?
Damage to superior laryngeal nerve --> loss of cricothyroid function (deepening of voice)
173
Ligation of inferior thyroid artery. Post surgical complication?
Damage to recurrent laryngeal nerve --> hoarseness
174
Hypocalcemia effects on ECG
QT Prolongation
175
what is most likely to be seen in a kidney biopsy in a patient with Primary Hyperparathyroidism?
Nephrocalcinosis of the renal tubules
HyperCa = metastatic calcification
176
Knuckle Knuckle Dimple Knuckle sign
Turners
177
Knuckle Knuckle Dimple Dimple sign
Pseudohypoparathyroidism (Albright heriditary dystrophy)
178
What is the specific defect in PsHP?
Defective Gs protein in the renal tubular cells --> kidney doesn't respond to PTH
(PsHP is to PTH as Nephrogenic DI is to ADH)
179
Which parent is responsible for passing on PsHP? Why?
Mom because of genetic imprinting
180
Pseudopseudohypoparathyroidism presentation
Look like albrights (short stature, short 4th/5th digits) but don't have end organ PTH resistance...PTH and Ca levels are normal
181
Which parent causes PsPsHP?
Father
182
Familial Hypocalciuric Hypercalcemia defect
Defective Ca Sensing receptor in the PTH means body can't respond to high Ca
183
FHH Labs (serum/urine Ca, PTH)
High serum Ca
High PTH
Low urine Ca
184
Relationship of Prolactinoma and Bone ina woman
Increases risk for osteoporosis
Prolactin inhibits GnRH = low estrogen = increased osteoclasti activity
185
2 enzymes implicated in Osmotic damage in diabetes
Aldose reductase
| ABSENCE of sorbitol dehydrogenase
186
Insulinoma Labs (glucose, insulin, Cpeptide)
Low glucose
High Insulin
High C peptide
187
Screening test (besides cpeptide) for insulinoma
Symptoms resolve after giving glucose, but then come back several hours later
188
Screening test for gastrinoma
Gastrin levels remain elevated after secretin administration
189
Potassium levels in primary vs secondary adrenal insufficiency. Why?
Low in Primary b/c entire adrenal is dead
Normal in secondary b/c ACTH doesn't directly stimulate the zona glomerulosa!!
190
Basis for CRH stimulation test in adrenal insufficiency
If CRH stimulates the production of new cortisol, the Dx is Secondary/tertiary adrenal insufficiency (b/c the pituitary wasn't releasing ACTH)
This is the same logic as in pituitary cushings vs ectopic ACTH production
191
Muscle disease in hypo vs hyperthyroid? how to differentiate?
Both get proximal muscle wekness
```
Hypothyroid = Increased CK
Hyperthyroid = Normal CK
```
