Endo USMLE Flashcards
1
Q
woman presents with diffuse goiter and hyperthyroidism. What are the expected values of TSH and thyroid hormones?
A
low TSH & hight thyroid hormones
2
Q
48y/o female presntes with progressive lethargy and extreme sensitivity to cold temperatures. What is the diagnosis
A
hypothyroidism
3
Q
pt with elevated serum cortisol levels undergoes a dexamethasone does not decrease cortisol levels, but 8 mg does. What is the dz?
A
pituitary tumor
4
Q
50y/o man complains of diarrhea. On physical exam his face is plethoric and a heart murmur is detected. What is the dx?
A
carcinoid syndrome
5
Q
woman of short stature presents with shortened 4th and 5th metacarpals. What endocrine d/o comes to mind?
A
Albright hereditary osteodystrophy or pseudohypoparathyroidism
6
Q
Nondiabetic pt presents with hypoglycemia but low levels of C pepetide. What is the dx?
A
Surreptitious insulin injection
7
Q
cortex of the adrenal glands comes from what embryologic source?
A
mesoderm
8
Q
medulla of the adrenal glands comes from what embryologic source?
A
neural crest
9
Q
GFR corresponds to
A
Salt (Na+)
Sugar (glucocorticoids) and
Sex (androgens)
mneu: the deepr you go the sweeter it gets
10
Q
What does GFR stand for?
A
zona glomerulosa
zona fasciculata
zona reticularis
11
Q
what does the zona glomerulosa secrete
A
aldosterone
12
Q
what is the primary regulatory control of the zona glomerulosa
A
renin-angiotensin
13
Q
what does the zona fasciculata secrete
A
cortisol, sex hormone
14
Q
what is the primary regulatory control of the zona fasciculata
A
ACTH, hypothalamic CRH
15
Q
what does the zona reticularis secrete
A
sex hormones (e.g., androgens)
16
Q
what is the primary regulatory control of the zona reticularis
A
ACTH, hypothalamic CRH
17
Q
what do the chromaffin cells cells of the medulla secrete
A
catecholamines (epi, NE)
18
Q
what is the primary regulatory control of the medulla
A
preganglionic sympathetic fibers
19
Q
what is the most common tumor of the adrenal medulla in adults
A
pheochromocytoma
20
Q
what is the most common tumor of the adrenal medulla in children
A
neuroblastoma
21
Q
out of pheochromocytoma and neuroblastoma which one causes episodic hyperension
A
pheochromocytoma
22
Q
how does the left adreanal gland drain blood
A
left adrenal ->left adrenal vein -> left renal vv -> IVC
23
Q
how does the right adreanal gland drain blood
A
right adrenal ->right adrenal vein -> IVC
24
Q
posterior pituitary is derived from what embryological origin
A
neuroectoderm
25
posterior pituitary secretes what
vasopressen and oxytoxin
26
where are vasopressen and oxytoxin made
hypothalamus
27
where are vasopressen and oxytoxin shipped
pituitary
28
where is the anterior pituatary derived from
oral ectoderm
29
what does the anterior pituitary secrete
FLAT Pig
```
FSH
LSH
ACTH, Melanotropin (MSH)
TSH
Prolactin
GH
```
30
alpha subunit is a common subunit to
TSH, LH, FSH, & hCG
31
Beta subunit determines this
hormone specificity
32
islet of Langerhans are collections of these three types of cells.
alpha, beta, delta cells
33
what part of the pancreas are the alpha, beta, & delta cells most numerous
tail
34
from where do the islets of Langerhans arise
pancreatic buds
35
alpha cells secrete
glucagon
36
beta cells secrete
insulin
37
delta cells secrete
somatostatin
38
prolactin ____ dopamine synthesis and secretion from the hypothalamus.
increases
39
dopamine subsequently _______ prolactin secretion
decreases
40
dopamine agonists (e.g., bromocriptine) ______ prolactin secretion. Dopamine antagonist (e.g., most antipsychotics) __________prolactin secretions.
decreases
| increases
41
in females prolactin inhibits_______ synthesis and release, which inhibits ovulation
GnRH
42
___________ this is commonly seen in prolactinomas
amenorrhea
43
what is the congenital adrenal hyperplasia: Female that is not maturing presents with HYPERTENSION, hypokalemia, she has decreased sex hormones, decrease cortisol, increased mineralocorticoids
17 alpha hydroxylase deficiency
44
this congenital adreanal hyperplasia is the most common form. It results in decreased cortisol (increased ACTH), decreased mineralocorticoids, increased sex hormones. Complications include masculinization, female psuedohermaphroditism, HYPOtension, hyponatremia, hyperkalemia, increased plasma renin activity, and volume depletion. Salt wasting can need to hypovolemic shock int he newborn
21 beta hydroxylase deficiency
45
this congenital adreanal hyperplasia results in low cortisol, low aldosterone and corticosterone and high sex horones. Complicatons include masculinization and (HYPERtension (11-deoxycorticosterone acts as a weak mineralocorticoid)
11 beta hydroxylase deficiency
46
where does PTH come from (cells and tissue)
chief cells of parathyroid
47
what are the 4 fxs of PTH
1) increased bone resorption of Ca++ & phosphate
2) increased kidney resorption of Ca++ in the distal convoluted tubule
3) decreased kidney resoption of phosphate
4) increased 1,25 (OH)2 vitamen D (cholecalciferol) production by stimulating kidney 1 alpha hydroxilase
mneu: PTH increases serum CA, decreases serum PO, increases urine PO4, and stimulates both osteoclasts and osteblasts
PTH: phosphate trashing hormone
48
what causes PTH secretion
decreased serum Ca++
49
image p. 250 actions of PTH and 1,25 OH D in maitenence of Ca++ & phosphate homeostasis
shown are the main actions of PTH & 1,25 (OH)2 D in the maintenance of Ca++ and phosphate homeostasis
50
source of vit D3
sun exposure in skin
51
source of D2
plants
52
where are D2 & D3 converted to 25 OH vit D
liver
53
where is 25 OH vit D converted to 1,25 (OH)2 vit D (active form)
kidney
54
what is the fx of vit D
1) increased absorption of dietary Ca++
2) increased absorption of dietary phosphate
3) increased bone resorption of Ca++ & (PO4)3-
55
what dz do you get if you don't get enough vit D (kids and adults)
kids-rickets
| adults-osteomalacia
56
what is 24,25-(OH)2 vit D
inactive form of vit D
57
in the regulation of vit D, what does increased PTH cause
increase 1,25-(OH)2 vit D formation
58
in the regulation of vit D, what does decreased [Ca++]cause
increase 1,25-(OH)2 vit D production
59
in the regulation of vit D, what does increased 1,25-(OH)2 vit D cause
increase 1,25-(OH)2 vit D inhibits its own production
60
What dz?
Ca++: ↑
Phosphate:↓
Alk Phos:↑
hyperparathyroidism
61
What dz?
Ca++: N/↑
Phosphate:N
Alk Phos:↑↑↑
paget's dz of bone
62
What dz?
Ca++: ↑
Phosphate:↑
Alk Phos:N/↑
vit D intoxication
63
What dz?
Ca++: N
Phosphate:N
Alk Phos:N
osteoporosis
64
What dz?
Ca++: ↓
Phosphate:↑
Alk Phos:N
renal insufficiency
65
where does calcitonin come from
parafolicular cells (C cells) of thyroid
66
what is the fx of calcitonin
↓ bone resorption of calcium
67
calcitonin opposes the action of what hormone
PTH
68
what stimulates calcitonin secretion
increased serum Ca++
69
the need for gene transcription and protein synthesis delays the onset of action of these steroid/thyroid hormones
mneu: PET CAT
```
Progesterone
Esterogen
Testosternone
Cortisol
Aldosterone
Thyroxine and T3
```
70
these hormones are lipophilic and insoluble in plasma; therfore, they must circulate bound to specific binding globulins, which increase solubility and allows for increased delivery of steroid to the target organ.
steroid
71
increased levels of sex hormone-binding globulin (SHBG) leads to lower levels of free testosterone and results in this physical exam finding
gynecomastia
72
decreased SHBG raises free testosterone leading to this finding
hirsutism
73
these are iodine containing hromones taht control the body's metabolic rate
thyroid hormones (t3/t4)
74
source of thyroid hormones
follicles of thyroid. Most T3 formed in the blood
75
fx of thyroid hormones
1) bone growth (synergism w/ GH
2) CNS maturation
3) beta adrenergic effects (increased CO,HR,SV, contractility
4) increase BMR via increased Na+/K+ ATPase activity -> increased O2 consumption, RR, increased body temp
5) increased glycogenolysis, gluconeogesis, lipolysis
```
mneu: T3 fx--4Bs
Brain maturation
Bone growth
Beta adrenergic effects
BMR incrase
```
76
what globulin binds most T3/T4 in blood
Throxine-binding globulin (TBG)
77
is free or bound thyroid hromone active
free
78
in what dz would you see decreased TBG
hepatic failure
79
in what condition would you see increase TBG
pregnancy
80
what hromone stimulates TSH secretion from the pituitary
TRH (hypothalamus
81
what cells does TSH stimulate to secrete thyroid hormone
follicular cells
82
negative feedback by this hormone to the anterior pituitary decreases sensititvity to TRH.
T3
83
in Graves dz it is this TSH analog that stimulates follicular cells
TSI
84
what organs depend on insulin for glucose uptake
skeletal mm and adipose tissue
85
what organs take up glucose independent of insulin levels (GLUT-1)
brain and RBC
86
what fuel can the brain use in starbation states
ketone bodies
87
this syndrome refers to increased cortisol levels due to a variety of causes. The clinical picture includes hypertension, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resistance), skin changes (thinning, striae), osteoporosis, amenorrhea, and immune suppression
cushing syndrome
88
If you're pt presents with cushings syndrome you have to identify the source, if the pt has increased ACTH levels because of a pituitary adenoma the pt has
Cushing's dz
89
If you're pt presents with cushings syndrome you have to identify the source, if the pt has decreased ACTH levels due to causes that are not iatrogenic, the pt has
primary adrenal hyperplasia/neoplasia
90
If you're pt presents with cushings syndrome you have to identify the source, if the pt has decreased ACTH levels due to iatrogenic causes, the pt may be taking
steroids (chronic)
91
describe the dexamethasone suppression test in a healthy person
low cortisol after low dose
92
describe the dexamethasone suppression test in a person with a ACTH-producing tumor
high cortosol after low dose; low cortisol after high dose
93
describe the dexamethasone suppression test in a person with a cortisone producing tumor
high cortisol after low and high dose
94
this dz is caused by an aldosterone-secreting tumor, resulting in HTN, hypokalemia, metabolic alkalosis, and LOW plasma renin
primary hyperaldosteronism (Conn's syndrome)
95
this dz is due to renal artery stenosis, chronic renal failure, cHF, cirrhosis, or nephrotic syndrome. Kidney perception of low intravascular volume results in an overactive renin0angiotensin system. Therefore, it is associated with HIGH plasma renin
secondary hyperaldosteronism
96
what is the tx for hyperaldosteronism
spironolactone (a K+ sparing diuretic that works by acting as an aldosterone antagonist)
97
this is a primary deficiency of aldosterone and cortisol due to adrenal atrophy, causing hypotension (hyponatremic volume contraction) and skin hyperpigmentation (due to MSH, a byproduct of increased ACTH production from POMC). It is characterized by Adrenal Atrophy and Absence of hormone production. It involves All 3 cortical divisions.
Addison's dz
98
How you distinguish Addison's dz (primary aldosterone/cortisol deficiency[renal problem]) from secondary aldosterone/cortisol deficiency [pituitary problem]
Secondary insufficency has no skin hyperpigmentation
99
this is the most common tumor of the adrenal medulla in adults. It is derived from chromaffin cells which arise from the neural crest
pheochromocytoma
100
what can pheochromocytomas be associated with if they occur in pts whith MEN types II & III
neurofibromatosis
101
this is the most common tumor of the adrenal medulla in children, but it can occur anywhere along the sympathetic chain
neuroblastoma
102
what do pheochromocytomas secrete
epi, NE, dopamine
103
how do you dx a pheo
urinary VMA and plasma catecholamines are elevated
104
what endocrine d/os are pheos assoc with
MEN types II & III
105
how do you tx pheos
alpha antagonists, especially phenoxybenzamine, a nonselective, IRREVERSABLE alpha blocker
106
symptoms of pheos occur in "spells"--meaning they often relapse and remit. What are the 5 "P"s of a pheo
```
Pressure (elevated BP)
Pain (headache)
Perspiration
Palpitations (tachycardia)
Pallor
```
107
give the rule of 10s associated with pheos
```
10% malignant
10% bilateral
10% extraadrena
10% calcify
10% kids
10% familial
```
108
this MEN type involves the 1) PANCREAS (e.g., Zollinger-Ellison syndrome, insulinomas, VIPomas) 2)PARATHYROID 3) PITUITARY TUMORS. It often presents with kidney stones and stomach ulcers
MEN I (Wermer's syndrome)= 3 "P" organs (Pancreas, Pituitary, and Parathyroidism)
109
this MEN type involves 1) MEDULLARY CARCINOMA OF THE THYROID 2)PHEOCHROMOCYTOMA 3) PARATHYROID TUMOR.
MEN type II (Sipple's syndrome)
110
this MEN type involves 1) MEDULLARY CARCINOMA OF THE THYROID 2)PHEOCHROMOCYTOMA 3) ORAL AND INTESTINAL GANGLIONEUROMATOSIS (MUCOSAL NEUROMAS).
MEN type III ( formerly MEN type IIb )
111
all MEN have this type of inheritance
autosomal dominant
112
what gene are MEN type II & III associated with
ret gene
113
this d/o often manifests itself with cold intolerance, hypoactivity, weight gain, fatigue, lethargy, decreased appitite, constipation, weakness, decreased reflexes, facial/periorbital myxedema, dry, cool skin, and coarse, brittle hairr
hypothyroidism
114
what will the labs show in hypothyroidism
increased TSH (most sensitive test for primary hypothyroidism)
decreased total T4
decreased free T4
decreased T3 uptake
115
in this dz the pt presents hypothyroid. It results because thyroid is replaced by fibrous tissue
Riedel's thyroiditis
116
this d/o manifests itself with heat intolerance, hyperactivity, weight loss, chest pain/palpitations, arrhythmias, diarrhea, increased reflexes, warm moist skin, and fine hair
hyperthyroidism
117
this is an autoimmune hyperthyroidism with thyroid stimulating/TSH receptor antibodies. It often presents during stress (e.g., childbirth) with opthalmopathy (proptosis, EOM swelling), pretibial myxedema, diffuse goiter.
graves dz
118
what type of hypersensitivity rxn in graves dz
type II
119
what lab results will you see in hyperthyroidism
decreased TSH (if primary)
increased total T4
increased free T4
increased T3 uptake
120
this is an autoimmune d/o resulting in hypothyroidism. It has a slow course and often you will see a moderately enlarged, nontender thyroid. Microscopically you will see a lymphocytic infiltrate with germinal genters. Pt will test positive for antimicrosomal and antithyroglobulin antibodies
Hashimoto's thyroiditis
121
this is a self-limited hypothyroidism which often follows a flulike illness. Pt will presents with jaw pain and a very tender thyroid gland. Labs will show signs of early inflammation and elevated ESR.
Subacute thyroiditis (de Quervain's)
122
this is the most common thyroid cancer. It has an excellent prognosis. Microscopically you will see "ground glass" nuclei and psammoma bodies
papillary carcinoma
123
this thyroid cancer has a good prognosis. microscopically you will see uniform follicules
follicular carcinoma
124
this thyroid cancer arises from parafollicular "C cells". It produces calcitonin. Microscopicallly you may see sheets of cells in amyloid stroma. It is seen in MEN types II & III
medullary carcinoma
125
this thyroid cancer occurs in older pts. It carries a very poor prognosis
undifferentiated/anaplastic
126
this occurs wherever endemic goiter is prevalent (lack of dietary iodine). It is common in china. It can also be caused by a defect in T4 formation or developmental failure in thyroid formation. You may see a pot-bellied, pale, puffy-faced child with protruding umbilicus and protuberant tongue
cretinism
127
adult pt presents with large tongue, deep furrows, deep voice, large hands and feet, coarse facial features, impared glucose tolerance (insulin resistance). What is the d/o and what hormone is in excess
acromegly
increased growth hormone
128
what does increased GH in children cause
gigantism
129
how do you tx increased GH either in acromegly or gigantism
octreotide
130
give some natural states in which you might have increased GH
stress, exercise, and hypoglycemia
131
this is usually caused by an ademona. labs will show hypercalemia, hypercalciuria (RENAL STONES), hypophosphatemia, increased, PTH & cAMP in urine. While it is often asymptomatic it may present with weakness and constipation ("GROANS")
primary hyperparathyroidism
132
this d/o is due to decreaesed serum Ca++, most often due to chronic renal dz. Labs will show hypocalcemia, hyperphosphatemia, and increased PTH
secondary hyperparathyroidism (hyperplasia)
133
this complication of primary hyperparathyroidism results when cystic bone speaces are filled with brown fibrous tissue causing BONE PAIN
Osteitis fibrosa cystica (von recklinghausen's syndrome)
134
this complication of secondary hyperparathyroidism, results in bone lesions due to renal dz
renal osteodystrophy
135
give the rhyme that describes hyperparathyroidism
stones, bones, and groans
136
pt presents with hypocalcemia or tetany. what dz
hypoparathyroidism.
137
give 2 causes of hypoparathyroidism
accidental surgical excision (thyroid sx)
DiGeorge syndrome
138
Chvostek's sign is a sign of hypoparathyroidism. What is it?
tap facial nn results in contraction of facial mm
139
trousseau's sign is a sign of hypoparathyroidism. What is it?
occlusion of brachial artery w/ BP cuff results in carpal spasm
140
pt presents w/ hypocalcemia, shortened stature and shortened 4th & 5th digits.
pseudohypoparathyroidism
141
what is pseudohypoparathyroidism
kidneys are unresponsive to PTH
142
what is the inheritance of pseudohypoparathyroidism
autosomal-recessive
143
give 5 causes of hypercalcemia
mneu: CHIMPANZEES
Calcium ingestion, Hyperparathyroid, Hyperthyroid,, Iatrogenic (thiazides, Multiple myeloma, Paget's dz, Addison's dz, Neoplasms, Zollinger-Ellison syndrome, Excess vit D, Excess vit A, Sarcoidosis
144
give some acute manifestations of diabetes mellitus
polydipsia, polyuria, polyphagia, weight loss, DKA (type 1), hyperosmolar coma (type 2), unopposed secretion of GH and epinephrine (exacerbating hyperglycemia)
145
image p. 256 --Diabetes mellitis
--
146
Give some chronic manifestations of Diabetes Mellitus
small vessel dz (diffuse thickening of basement membrane) ->retinopathy (hemorrhage, exudates, microaneurysms, vessel proliferation), claucoma, nephropathy (nodular sclerosis, progressive protinuria, chronic renal failure, arteriosclerosis leading to HTN)
2. Large vessel atherosclerosis, CAD, peripheral vascular occlusive dz and gangrene, cerebrovascular dz
Neuropathy (motor, sensory, and autonomic degeneration)
Cataracts (sorbitol accumulation
147
what tests should you run in dbts
fasting serum glucose
glucose tolerance test
HbA1c
148
what does HbA1c meausre
long term diabetic control
149
what is the primary defect in type 1--juvenile onset (IDDM)
viral or immune destruction of beta cells
150
what is the primary defect in type 2--adult onset (NIDDM)
increased resistance to insulin
151
is insulin necessary for tx in type 1--juvenile onset (IDDM)
always
152
is insulin necessary for tx in type 2--adult onset (NIDDM)
sometimes
153
at what age does type 1--juvenile onset (IDDM)usually strike [many exceptions]
<30
154
at what age does type 2--adult onset (NIDDM)usually strike [many exceptions]
>40
155
is type 1--juvenile onset (IDDM)associated with obesity
no
156
is type 2--adult onset (NIDDM)associated with obesity
yes
157
is there a genetic predisposition to type 1--juvenile onset (IDDM)
weak, polygenic
158
is there a genetic predisposition to type 2--adult onset (NIDDM)
strong, polygenic
159
is there an HLA association to type 1--juvenile onset (IDDM)
yes (HLA-DR3 &4)
160
is there an HLA association to type 2--adult onset (IDDM)
no
161
describe the glucose intolerance associated with type 1--juvenile onset (IDDM)
severe
162
describe the glucose intolerance associated with type 2--adult onset (NIDDM)
mild-moderate
163
Is ketoacidosis associated with type 1--juvenile onset (IDDM)
commonly
164
Is ketoacidosis associated with type 2--adult onset (NIDDM)
rarely
165
describe the beta cell numbers in the islets associated with type 1--juvenile onset (IDDM)
low
166
describe the beta cell numbers in the islets associated with type 2--adult onset (NIDDM)
variable
167
describe the serum insulin associated with type 1--juvenile onset (IDDM)
low
168
describe the serum insulin associated with type 2--adult onset (NIDDM)
variable
169
are the classic symptoms of polyuria, polydipsia, thirst, and weight loss associated with type 1--juvenile onset (IDDM)
commonly
170
are the classic symptoms of polyuria, polydipsia, thirst, and weight loss associated with type 2--adult onset (NIDDM)
sometimes
171
diabetic ketoacidosis is one of the most important complications of type 1 dbts describe its pathology
excess fat breakdown and increased ketogenesis from increase in free fataty acids, which are then made into ketone bodies.
172
what is ketoacidosis usually due to
an increase in insulin requirements due to an increase in stress (e.g., infection)
173
give some signs and symptoms of diabetic ketoacidosis
kussmaul respirations (rapid/deep breathing), hyperthermia, nausea/vomiting, abdominal pain, psychosis/dementia, dehydration. Fruity breath odor (due to exhaled acetone)
174
what will the labs of a pt in diabetic ketoacidosis show
hyperglycemia, increase H+, decreased HCO3-, (anion gap metabolic acidosis, increased blood ketone levels, leukocytosis. Hyperkalemia, but depleted intracellular K+
175
what are some complications of diabetic ketoacidosis
life-threatening mucormycosis, rhizopus infxn, cerebral edema, cardiac arrhythmias, heart failure
176
how do you tx a pt in diabetic ketoacidosis
fluids, insulin, and potassium; glucose if necessary to prevent hypoglycemia
177
this d/o is characterized by intensive thirst and polyuria together with aninability to concentrate urine owing to lack of ADH
diabetes insipidus
178
this type of diabetes insipidus may be caused by a pituitary tumor, trauma, surgery, histiocytosis
central DI
179
this type of diabetes insipidus may be caused by hereditary factors, hypercalcemia, lithium, demeclocycline
nephrogenic DI (lack of renal response to ADH)
180
how do you dx DI
water deprivation test --urine specific gravity 290mOsm/L
181
how do you tx central DI
intranasal despopressin (ADH analog
182
how do you tx central DI
hydrochlorothiazide, indomethacin, or amiloride
183
this d/o results in
1) excessive water retention
2) hyponatremia
3) urine osmolarity>serum osmolarity
syndrome of inappropriate antiduiuretic hormone secretion
184
how do you tx SIADH
demeclocycline or H2O restriction
note: tx slowly
185
in SIADH very low serum sodium levels can lead to this
seizures
186
give some causes of SIADH
1) ectopic ADH (small cell lung CA)
2) CNS disorders/head trauma
3) pulmonary dz
4) Drugs (e.g., cyclophosphamide)
187
this is a rare syndrome that results in recurrent diarrhea, cutaneous flushing, asthmatic wheezing, and right sided valvular dz.
carcinoid syndrome
188
what will you find in the urine of a pt with carcinoid syndrome
increased 5-HIAA in urine
189
carcinoid tumor is the most common tumor in this part of large intestine
appendix
190
carcinoid tumors result from this type of cell
neuroendocrine cells
191
carcinoid tumor secretes high levels of this
5-HT (seratonin)
192
if carcinoid tumor is limited to here you wont see symptoms
GI tract
| 5-HT undergoes 1st pass metabolism in liver
193
give the rule of 1/3 for carcinoid tumors
1/3 metastasize
1/3 present w/ 2nd malignancy
1/3 multiple
194
where to carcinoid tumors derive from
neuroendocrine cells of GI tract
195
how do you tx carcinoid tumors
octreotide
196
this is a gastrin secreting tumor of pancreas or duodenum. It causes recurrent ulcrs
Zollinger-Ellison syndrome
197
what MEN syndrome is ZE syndorme associated with
MEN type I
198
what is the tx strategy for type 1 DM
low sugar diet, insulin replacement
199
what is the tx strategy for type 2 DM
dietary modification, exercise for weight loss, and oral hypoglycemics
