Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

System Path II > Endocrine > Flashcards

Endocrine Flashcards

1
Q

storage form of insulin?

A

proinsulin

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

normal fasting blood glucose? diabetic?

A

4-6 mmol/L

>7 (126 mg/dL)

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

normal random blood glucose? diabetic?

A

< 9 mmol/L

>11.1 (200 mg/dL)

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

name 3 endogenous hormones that antagonize insulin

A

cortisol
growth hormone
catecholamines

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

name 2 genetic diseases associated with diabetes

A

Down’s

Turner’s

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

what is the differential age for onset between diabetes type I and II?

A

40
< 40 = type 1
> 40 = type 2

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

which type of diabetic presents with ketoacidosis? why doesn’t the other type?

A

type 1

type 2 have insulin which is very antiketogenic

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

Which type of diabetes has an established HLA link? what is the HLA involved?

A

type 1
HLA-DR3 & HLA-DR4
DQA1 & DQB1

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

coxsackie B4 virus is associated with what disease?

A

Diabetes Type I

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

Rubella and mumps are associated with what disease?

A

Diabetes Type I

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

which type of diabetes has a long pre-diabetic phase? What symptoms do they exhibit? What is found in their blood?

A

Type I
asymptomatic
islet cell antibodies (ICA)

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

name 2 possible etiologies of type I diabetes

A

viral infection and molecular mimicry

direct damage to beta cells

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

which type of diabetes has the strongest genetic component?

A

type II

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

name 2 compounds found in obese patients and explain how they lead to the development of diabetes

A

Obese patients have high levels of FAs and TNF (both produced by adipose tissue) and they are both insulin antagonists

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

which diabetes is associated with amyloid? why?

A

Type II

it is secreted with insulin and type I diabetics don’t produce insulin

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

explain vomiting in diabetes

A

in type I diabetics, production of ketone bodies is high, ketones stimulate the area postrema responsible for vomiting

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

is high urine glucose diagnostic for diabetes? why or why not?

A

No, used for screening only

Diagnosis is based off of HbA1C > 6.5%

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

how could a severely diabetic patient present with normal HbA1C levels?

A

If they have HbS or HbF from sickle cell or thalassemia the % of HbA will be skewed

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

explain the term “impaired fasting glycemia” (IFG)

A

prediabetic state where fasting glucose levels are above normal but below diabetic range (between 5.6 and 6.9 mmol/L)

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

explain the term “impaired glucose tolerance” IGT

A

prediabetic state where the 2h value of the OGTT (oral glucose tolerance test) is above normal, but below diabetic range (between 7.8 and 11.1mmol/L)

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

explain how hyperglycemia can lead to dehydration

A

glucose is freely filtered, but cannot all be reabsorbed like it is normally. It is osmotically active and draws water into filtrate -> polyuria, dehydration

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

explain how diabetics can develop lactic acidosis

A

caused by dehydration and vasoconstriction by stress hormones (from cellular starvation and hypovolemia)

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

what two substances do you give to someone with ketoacidosis? why?

A

insulin to encourage cellular uptake of glucose

potassium to fix electrolyte imbalance from vomiting and osmotic diuresis

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

75 year old, very dehydrated woman presents to the ER in a comatose state, there is no sign of ketoacidosis. explain her situation and what is characteristic of her blood work?

A

She is a type 2 diabetic in a hyperosmolar nonketotic coma. She has enough insulin to suppress ketosis, but cannot suppress hyperglycemia. Her blood will show VERY high glucose levels which is causing the dehydration by glucose’s osmotic action in the renal filtrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is the first long term complication of diabetes to present in microangiopathy? what are 3 common complications of diabetic microangiopathy?

A

thickening of the basement membrane

retinopathy, nephropathy, neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is the most common complication of diabetic macroangiopathy and how does it present?

A

atherosclerosis

ischemic heart disease, stroke, peripheral vascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

most important treatment in long term diabetics is?

A

prevention of vascular accidents, even more important than controlling blood glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

list the first functional change, first biochemical sign, and first morphological signs seen in diabetic nephropathy

A

functional: hyperfiltration
biochemical: microalbuminuria
morphological: thickening of basement membrane and mesangial expansion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the most common cause of blindness in adults 30-65 years old?

A

diabetic retinopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

name 3 long term complications involving the eye in diabetics

A

retinopathy
cataracts
glaucoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

explain AGE and give a complication

A

advanced glycosylation end products in diabetics

high blood glucose leads to glycosylation of basement membranes capillaries and structural proteins -> retinopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

explain why cataracts form in diabetics

A

lens does not require insulin for glucose uptake, gets a lot, glu is shuffled into minor metabolism pathways because glycolysis is overwhelmed. Gets converted into sorbitol which is highly osmotically active and accumulation leads to discoloration of lens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

explain the major differences of a histo section of the pancreas between type I and type II diabetes. What is common to both?

A

type I: lymphocytic infiltration
type II: amyloid deposition
both: pancreatic hyalinization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

give 3 early changes in the kidney with diabetes

A

basement membrane thickening
mesangial cell proliferation
hyaline arteriolosclerosis of afferent and efferent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

give 2 later appearances of the kidney associated with diabetes. Which is more specific for diabetes? In what other pathology can the other change be seen?

A

diffuse mesangial sclerosis
nodular glomerulosclerosis

Nodular is specific to diabetes, diffuse can be seen in old age and hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

on histology of a kidney biopsy you find spherical deposits of laminated matrix. what are these deposits? How do they stain? What disease are they associated with?

A

Kimmelstiel wilson lesions
PAS+
diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

your kidney biopsy is described as having a finely granular cortical surface. What pathology is involved? Associated with what disease?

A

this describes a scarred kidney caused by long term ischemia. Commonly seen in nodular glomerulosclerosis of diabetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is the hallmark of proliferative retinopathy in diabetics?

A

neovascularization and fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

explain the pathogenesis of microaneurysms in diabetic retinopathy

A

loss of pericytes (sorbitol is toxic to them and glucose freely enters pericytes) that provide structural support to capillaries leads to ballooning and possible rupture of the vessels of the eye

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

why would a diabetic present with hyperkalemia? When would you see hypokalemia?

A

insulin drives K+ into cells, so type I diabetics have no insulin so K+ stays in blood

hypokalemia is seen after treatment with insulin and a reversal of acidosis. K+ is driven into the cells and patient can become hypokalemic without supplementation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

explain how type II diabetics can present with coma

A

high glucose leads to life-threatening diuresis and if dehydration is severe enough, the hypotension can result in coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

explain the pathogenesis behind peripheral neuropathy in diabetics

A

glucose can freely enter Schwann cells which myelinate peripheral nerves. Production of sorbitol leads to osmotic damage and death of schwann cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

explain the importance of the blood supply to the anterior pituitary

A

Not very well oxygenated - very susceptible to infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

which hormones are produced by acidophils in the ant. pituitary? name the ones produced by the basophils

A

Acidophil: growth hormone - prolactin
Basophil: TSH - ACTH - LH - FSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

GnRH triggers the release of what hormones?

A

LH and FSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

CRF triggers the release of what hormones?

A

ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

TRH triggers the release of what hormones?

A

TSH and prolactin

TRH = thyrotrophin releasing hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

which molecule inhibits the release of growth hormone?

A

somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what molecule triggers the release of growth hormone?

A

GH-RH (growth hormone releasing hormone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the functionality of the most common pituitary disorder? What causes it? How?

A

hypopituitarism

pituitary adenoma - as it expands, it destroys other secreting cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

a woman has a complicated pregnancy and loses a lot of blood during birth and becomes severely hypovolemic. what is she at risk for? what is this called? why?

A

hypopituitarism
Sheehan’s syndrome
pituitary enlarges during pregnancy and becomes even more vulnerable to ischemia/infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

a woman experiences low milk production after giving birth - give a possible differential

A

Sheehan’s syndrome - hypopituitarism due to infarct from loss of blood during delivery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

name two diseases associated with hypopituitarism

A

sarcoidosis

hemochromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

pt seems to be experiencing symptoms of hypopituitarism but her LH is normal. what does this tell you? why?

A

probably not hypopituitarism because LH and GH are the first deficiencies to appear in hypopituitarism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

List the hormones of the anterior pituitary in the order that they present in deficiency. Starting with the one that generally becomes deficient first

A

disappears first: LH, GH

next: FSH
last: ACTH, TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

a female presents with menstrual disturbances and delayed puberty - give a differential

A

loss of gonadotrophins - LH and FSH

hypopituitarism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

a male is experiencing loss of libido, loss of facial and body hair, and impotence - give a differential

A

loss of gonadotrophins - LH and FSH

hypopituitarism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is a complication of panhypopituitarism?

A

coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

name the stress hormones released by the anterior pituitary. How do you asses their release?

A

prolactin
GH
ACTH

induce a stress, hypoglycemia, by injecting patient with insulin and measure levels released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

antipsychotics and oral contraceptives have what affect on the pituitary?

A

hyperprolactinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what is the most common pituitary tumor?

A

prolactinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

renal failure has what effect on the pituitary? why?

A 
hyperprolactinemia
excess release (its a stress hormone) and reduced clearance because its usually metabolized in the kidney
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

female presents with amenorrhea, infertility, and galactorrhea - differential?

A

hyperprolactinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

patient presents with frontal bossing, hypertension, arthritis, loss of libido, and symptoms of diabetes mellitus - differential? cause? explain

A

Acromegaly - excess GH release after childhood due to adenoma

diabetes: GH antagonizes insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

GH inhibits action of what other hormone?

A

insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

When would you measure IGF-1 levels and why?

A

insulin-like growth factor-1

acromegaly - GH acts on liver to produce IGF-1 and it is more stable than GH so easier to measure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What should happen to GH levels after the administration of oral glucose? Failure of this to happen suggest what?

A

normal person should show undetectable levels of GH following glucose (GH antagonizes insulin which needs to be high, so GH release is inhibited)

if GH levels are normal or paradoxically rise -> acromegaly (ant. pituitary adenoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

When is ADH secreted (2)?

What does it cause? How?

A

secreted in response to decreased blood volume or raised plasma osmolality

causes water retention by increasing permeability in the distal convoluted tubules and collecting ducts in the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

patient presents with polyuria and polydipsia, and is extremely dehydrated - differential? causes (2)?

A

diabetes insipidus
Central: lack of ADH
Nephrogenic: resistance to ADH action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

name 2 metabolic causes of diabetes insipidus

A

hypokalemia

hypercalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

explain the water deprivation test and what disease it’s used to diagnose

A

fluid restriction for 8 hours, pee every hour, measure urine volume and osmolality and body weight - if the urine does not become concentrated, indicates diabetes insipidus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

how can you differentiate between central and nephrogenic diabetes insipidus?

A

after fluid deprivation and the urine osmolality stays low, give ADH - urine osmolality will increase if central, and won’t change if nephrogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

patient presents with coma, water retention, and hyponatremia - differential?

A

SIADH - excess secretion of ADH with no feedback

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what hormone is most responsible for reabsorbing sodium in the collecting tubule?

A

aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

explain why patients with SIADH have hyponatremia yet still lose it in their urine

A

excess ADH leads to water retension -> hypervolemia. The main hormone responsible for reabsorption of sodium in the collecting tubule is aldosterone, but it is only released during hypovolemia, so sodium is lost in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what hormone suppresses prolactin production?

A

dopamine

77
Q

prolactin inhibits synthesis and release of what? associated symptoms?

A

GnRH so no FSH or LH -> amenorrhea

78
Q

explain the relationship between GH adenoma and secondary diabetes mellitus

A

GH decreases glucose uptake by cells but also induces liver gluconeogensis -> high blood glucose

79
Q

desmopressin is an analog of what? used to treat what?

A

analog of ADH

treats central diabetes insipidus

80
Q

Male with a history of smoking presents with a poorly differentiated, centrally located tumor in his lungs. What other disease can be associated with this condition?

A

Small cell carcinoma, releases ADH -> SIADH

81
Q

name the 2 thyroid hormones and which is produced in greater abundance?

A

Most: T4 - thyroxine

T3 - tri-iodothyronine

82
Q

name two major functions of thyroid hormones

A

stimulate basal metabolic rate

inc. sensitivity of CVS and nervous system to catecholamines by upregulating B1 receptors

83
Q

what two hormones are necessary for release of thyroid hormone? also give their locations of production

A

TRH from hypothalamus

TSH from pituitary

84
Q

Pt presents with infertility, arrythmias, osteoporosis and muscle weakness - differential? other associated symptoms?

A

Hyperthyroidism

exophthalmos, lid lag, weight loss, tachycardia, sweating, diarrhea

85
Q

what do the C cells of the thyroid produce? what is its function?

A

calcitonin - reduces serum calcium, opposes PTH

86
Q

pt. presents with hypocholesterolemia, hypercalcemia, and hyperglycemia - differential?

A

hyperthyroidism

87
Q

35 year old female presents with a diffuse enlargement in her neck and periorbital edema - what is characteristic on histology (2)?

A

graves disease - hyperthyroidism

scalloping of colloid, chronic inflammation

88
Q

pretibial myxedema - diagnosis? what type of hypersensitivity? explain pathogensis

A

Grave’s disease - hyperthyroidism
type II hypersensitivity
IgG autoantibodies that stimulate TSH receptor

89
Q

elevated T4
decreased TSH
hypocholesterolemia
hyperglycemia

A

Graves disease - hyperthyroidism

90
Q

following viral infection, patient presents with weight loss, exophthalmos, pain, tenderness in neck, and fever - explain current symptoms and course of his illness

A

Subacute DeQuervain’s thyroiditis
inflammation post viral infection destroys acini of thyroid gland leading to release of premade thyroid hormone and hyperthyroidism symptoms. It is self limiting, does not progress to hypothyroidism

91
Q

patient presents with multinodular, nontoxic goiter - differential? cause?

A

euthyroid enlargement due to iodine deficiency

92
Q

decreased T4
elevated TRH
elevated TSH

A

iodine deficiency

93
Q

patient presents with carpal tunnel syndrome, infertility, and hyperprolactinemia - differential? cause for hyperprolactinemia?

A

hypothyroidism
thyroid hormone is not being produced, no negative feedback on hypothalamus, leading to increased TRH which is responsible for release of both TSH and prolactin

94
Q

HLA-DR5 - disease?

A

Hashimoto thyroiditis (hypothyroidism)

95
Q

thyroid biopsy shows fleshy, soft, pale, lobular nodules protruding above the cut surface with areas of depression between the nodules - disease? what is the explanation for the areas of depression? what is an important disease association with this condition?

A

Hashimoto’s thyroiditis (hypothyroidism)

depressed areas are fibrosis from autoimmune destruction of the gland

association: increased risk for B-cell (marginal zone) lymphoma

96
Q

how do you differentiate between the early stages of Hashimoto’s thyroiditis and subacute De Quervain thyroiditis based on symptoms alone?

A

Both present initially as hyperthyroidism due to destruction of the gland and release of preformed thyroid hormone. However, Hashimoto’s will progress to hypothyroidism whereas De Quervain’s is self limiting and will not progress

97
Q

neonate presents with a protruding tongue, umbilical hernia, and shows signs of mental retardation - diagnosis? give 3 possible causes

A

Cretinism - hypothyroidism

maternal hypothyroidism during pregnancy
thyroid agenesis (DiGeorge!)
iodine deficiency
98
Q

patient presents with muscle weakness, bradycardia, hypercholesterolemia and constipation - diagnosis? 3 possible causes?

A

hypothyroidism

iodine deficiency, Hashimoto’s thyroiditis, radioablation of thyroid

99
Q

On serology you find anti-TPO and antithyroglobulin antibodies from your patient’s blood. Diagnosis? what is characteristic of this condition on histology? describe

A

Hashimoto’s thyroiditis

germinal centers and Hurthle cells (eosinophilic metaplasia of cells that line follicles)

100
Q

what two values do you need to investigate to fully analyze the state of thyroid function?

A

TSH and T4

101
Q

46 year old woman complains of hot flushes and presents with diffusely enlarged thyroid.
TSH levels are high, and T4 levels are on the low end of normal. Differentials?

A

Early hypothyroidism (presents with hyperthyroid symptoms first from release of thyroid hormone from destruction of follicles)

mild iodine insufficiency

102
Q

elderly woman is noted to have high TSH levels but normal levels of T4/T3 and is otherwise asymptomatic - diagnosis? 2 complications

A

sub-clinical hypothyroidism (usually in elderly - page 32 of class notes)

can convert to hypothyroidism
associated with endothelial dysfunction -> atheroma

103
Q

what is the effect of GH on blood glucose levels?

A

GH inhibits uptake of glucose by cells -> high blood sugar

104
Q

patient presents with hyperglycemia, hypertension, osteoarthritis, headache, and prognathism - diagnosis? most common cause of death?

A

acromegaly

death due to cardiac failure (GH leads to organ enlargement too)

105
Q

explain “hot” vs “cold” nodules - which is associated with adenoma? Grave’s? carcinoma?

A

hot nodule actively produces thyroid hormone so shows increased uptake of radioactive iodoine. cold nodules dont produce hormone and so decreased uptake of radioactive iodine

hot nodules: Grave’s
cold nodules: adenoma (but can rarely secrete thyroid hormone) and carinoma

106
Q

Patient with a history of ionizing radiation exposure presents with mass in his neck and enlargement of several cervical lymph nodes. Diagnosis? What is characteristic on histo? Prognosis?

A

Papillary carcinoma of the thyroid

Orphan Annie eye nuclei (clear) and psammoma bodies

excellent prognosis even with lymph node involvement

107
Q

on histology of thyroid biopsy you see outpouchings of the stroma lined by cells showing finely dispersed chromatin - diagnosis? how common?

A

Papillary carcinoma of the thyroid

most common thyroid carcinoma, but thyroid adenoma is far more common

108
Q

On fine needle aspiration of a singular nodular lesion of the thyroid, you find well differentiated follicles. Patient also shows masses in lung and liver - diagnosis? what is unique? treatment

A

Follicular carcinoma of the thyroid
carcinoma that spreads hematogenously (other 3 exceptions are renal cell, hepatocelluar, and choriocarcinoma)

responds to TSH so give thyroid hormone to inhibit release of endogenous TSH

109
Q

nodule of the thyroid shows increased uptake of radiolabeled iodine. Should you be concerned? Why or why not?

A

No, carcinoma usually results in loss of function (cold nodules) so uptake of iodine indicates a functioning gland and is less likely to be cancer

110
Q

on biopsy of thyroid you find concentric layers of calcification and extensions of stroma with a fibrovascular core with multiple layers of cuboidal and columnar cells - diagnosis? mutation involved?

A

Papillary carcinoma of the thyroid

RET and RAS pathway mutations

111
Q

where does papillary carcinoma of the thyroid commonly spread? how?

A

cervical lymph nodes via lymph

112
Q

where does follicular carcinoma of they thyroid common spread? how?

A

liver, bone, lung

hematogenously

113
Q

patient presents with mass in his neck and hypocalcemia - diagnosis? what cells are involved? pathogenesis of the hypocalcemia?

A

Medullar carcinoma of the thyroid
parafollicular C cells - they secrete calcitonin which is inactive at normal physiological levels, but increased levels from tumor can lead to hypocalcemia by increasing renal excretion of calcium

114
Q

biopsy of the thyroid gland shows sheets of malignant cells on a glassy pink background - diagnosis? most common hereditary cause? mutation? treatment?

A

medullary carcinoma of the thyroid
MEN 2A and 2B
RET mutation
detection of RET mutation -> prophylactic thyroidectomy (also treatment)

115
Q

what feature is most important in diagnosis of follicular carcinoma of the thyroid? why?

A

must do biopsy to find capsular invasion - otherwise, the stroma looks like normal thyroid gland

116
Q

on histo of thyroid biopsy you see nests of polygonal to spindle-shaped cells - diagnosis?

A

medullary carcinoma of the thyroid

117
Q

patient presents with moon face, buffalo hump, watery diarrhea, and cervical lymphadenopathy - diagnosis? explain the pathogenesis of this condition? what is another possible association?

A

Medullar carcinoma of the thyroid
ACTH is also secreted by the tumor along with calcitonin resulting in cushing’s symptoms

patient could also present with carcinoid syndrome due to tumor producing serotonin as well

118
Q

patient presents with flushing, watery diarrhea, and a mass in her neck - diagnosis? what is found in urine?

A

medullary carcinoma of the thyroid causing paraneoplastic syndrome (carcinoid syndrome from production and release of serotonin)

5-HIAA is found in urine - breakdown product of serotonin

(flushing is key feature of carcinoid syndrome)

119
Q

73 year old woman presents with dysphagia and trouble breathing and a firm, bulky, enlarging mass in her neck - diagnosis? prognosis? how do cells appear on histo?

A

anaplastic carcinoma of the thyroid

very poor prognosis, most malignant tumor in the body (only in people over 60)

cells are undifferentiated, pleomorphic, anaplastic

120
Q

scalloping of colloid is involved with which type of nodule in the thyroid? hot or cold? why is this important?

A

only seen in hot - malignancy is virtually nonexistent in hot nodules

121
Q

most common swelling of thyroid gland?

A

thyroid adenoma - benign

122
Q

name the 3 zones of the adrenal gland and the major hormone produced by each

A

glomerulosa: aldosterone (mineralcorticoids)
fasiculata: cortisol (glucocorticoids)
reticularis: testosterone (androgens)

123
Q

17-alpha hydroxylase deficiency leads to a decrease in the production of what? increase in what? give characteristics

A

decrease in: androgens and cortisol
increase in: aldosterone

feminine, hypertension

124
Q

21-beta hydroxylase deficiency leads to a decrease in the production of what? increase in what? give characteristics

A

decrease in: aldosterone and cortisol
increase in: androgens

masculinity, hyponatremia, hyperkalemia, hypovolemia, hypotension

125
Q

which hormone is an insulin antagonist and an anti-inflammatory?

A

cortisol

126
Q

which hormone increases sodium reabsorption in the kidney in exchange for potassium and hydrogen ions?

A

aldosterone

127
Q

which group of hormones leads to precocious puberty in boys and masculinization of females?

A

androgens

128
Q

release of cortisol from adrenal glands is regulated by the action of what two hormones?

A

hypothalamus: CRH
pituitary: ACTH

129
Q

what hormone’s release follows the circadian rhythm? when are concentrations highest? lowest? what can override this pattern?

A

cortisol
highest: morning
lowest: midnight
stress can override

130
Q

name the two physiological conditions that lead to release of aldosterone

A 
hypotension
sodium loss (hyponatremia)
131
Q

what hormone controls the release of androgens?

A

ACTH

132
Q

young child presents with very high fever, tachypnea, and petechiae on his extremities - diagnosis? associated pathological process? complication from this associated process?

A

sepsis (most commonly N. meningitidis)

Waterhouse-Friderichsen syndrome

W-F syndrome leads to hemorrhagic necrosis of the adrenal glands bilaterally which leads to a lack of cortisol - lack of cortisol exacerbates hypotension from sepsis and can lead to death

133
Q

patient presents with hypotension, hypovolemia, hyperkalemia and hyperpigmentation - diagnosis? most common cause in developed world? developing world? other?

A

adrenal insufficiency

developed: autoimmune destruction (Addison’s)
developing: TB
other: metastasis from lung cancer (lung cancer loves to go to adrenals)

134
Q

which hormone is associated with hyperpigmentation? is it due to lack of or excess hormone?

A

ACTH

excess (increased ACTH by-products stimulate melanocytes)

135
Q

what cancer has a common metastasis to the adrenal gland?

A

lung cancer

136
Q

patient presents with tiredness, anorexia, abdominal pain, hyperpigmentation and postural hypotension - diagnosis?

A

Addison’s

137
Q

how do you tell the difference between primary adrenal insufficiency (Addison’s) and secondary adrencortical insufficiency (pituitary problem) based on presentation?

A

secondary does not present with hyperpigmentation (no ACTH) and, initially, no electrolyte disturbances due to presence of aldosterone (released from renin-angiotensin system, not pituitary)

138
Q

explain the synacthen test - what is it testing?

give 2 conditions it used for

A

you give ACTH analog (synacthen) to see if cortisol is produced - tests residual capacity of the adrenal gland

  1. it can differentiate between addisons and secondary adrenal insufficiency based on whether the gland responds to ACTH with cortisol production or not
  2. it can be used to test for 21-hydroxylase deficiency - if it is deficient, the ACTH analog will lead to production of excess androgens so you would see elevated 17-alpha hydroxyprogesterone in blood
139
Q

patient presents with hypertension, frequent colds, muscle weakness and abdominal striae - diagnosis? explain the pathogenesis behind each of the presenting symptoms

A

hypercortisolism (cushings)

hypertension: cortisol upregulates alpha-1 receptors on arterioles (inc. peripheral resistance)
frequent colds: cortisol is an immune suppressant
muscle weakness: cortisol breaks down muscles for gluconeogensis
striae: cortisol inhibits collagen synthesis

140
Q

explain the mechanism behind the moon facies, buffalo hump, and truncal obesity (what disease?)

A

cushing’s

cortisol breaks down muscle for gluconeogenesis leading to hyperglycemia - this stimulates production of insulin which increases storage of fat

141
Q

name two important sources of ectopic ACTH

A 
small cell lung carcinoma
steroid usage (iatrogenic)
142
Q

briefly explain the low-dose dexamethasone suppression test - what is it used for?

A

dexamethasone is a cortisol analog that suppresses ACTH production, used to diagnose the potential cause of hypercortisolism

143
Q

dexamethasone suppression test shows no suppression at low levels, but suppression at high levels - what does this indicate?

A

Cushing’s disease (pituitary tumor)

144
Q

dexamethasone suppression test shows no suppression at low or high levels - what does this indicate?

A

ACTH production by small cell lung carcinoma

or cortisol secreting tumor of adrenal gland

145
Q

what is the only cause of hypercortisolism in which you seen unilateral atrophy of the adrenal gland? explain

A

primary cortisol secreting tumor of the adrenal gland - excess cortisol inhibits ACTH release from pituitary thus leading to down regulation of cortisol production by functional adrenal gland, eventually leading to atrophy

146
Q

what is the only cause of hypercortisolism where you see bilateral atrophy of the adrenal gland? explain

A

exogenous use of corticosteroids - steroids suppress ACTH secretion via negative feedback, leading to down regulation of cortisol production by the adrenal glands, eventually leading to atrophy

147
Q

patient presents with hypertension, hypernatremia, hypokalemia, and metabolic alkalosis - diagnosis?

A

hyperaldosteronism (Conn syndrome)

148
Q

explain aldosterone’s actions on the kidney

A

increases sodium absorption, potassium secretion and hydrogen ion secretion at the distal tubules and collecting duct

149
Q

patient presents with hypertension. Plasma cortisol in the morning is 470 nmol/L and at midnight is 110 nmol/L - what can you rule out as the cause of her hypertension and why

A

cannot be due cushings because the cortisol levels follow the circadian rhythm - they would always be high in cushings

150
Q

girl presents with enlarged clitoris and partially fused labia - diagnosis?

A

21-beta hydroxylase deficiency

congenital adrenal hyperplasia

151
Q

female patient presents with hirsutism and infertility - diagnosis?

A

21-beta hydroxylase deficiency

late onset congenital adrenal hyperplasia

152
Q

teenage girl presents with delayed puberty, no breast development, and amenorrhea - diagnosis? what would be an associated symptom? why?

A

17-alpha hydroxylase deficiency
(congenital adrenal hyperplasia)

hypertension due to excess mineralocorticoid production

153
Q

what is the breakdown product of catecholamines? what two enzymes are used to degrade them?

A

VMA (Vanillyl mandelic acid)

COMT and MAO

154
Q

from what cell type are chromaffin cells produced? where are they found? what do they produce?

A

neural crest cells
adrenal medulla
catecholamines

155
Q

what are the 3 tumors associated with MEN2a? what gene is mutated?

A

medullary carcinoma of the thyroid
pheochromocytoma
parathyroid adenoma

RET

156
Q

what are the 3 tumors associated with MEN2b? what gene is mutated?

A

medullary carcinoma of the thyroid
pheochromocytoma
ganglioneuromas of the oral mucosa

RET

157
Q

explain the rule of 10s

A 
pheochromocytoma
10% inherited (90% sporadic)
10% malignant (90% benign)
10% bilateral (90% unilateral)
10% component of MEN2a/MEN2b
10% in childhood (90% in adulthood)
10% found outside adrenal medulla
10% have no assoc. hypertension
158
Q

pheochromocytoma presents with vascular invasion. Is it malignant? why or why not?

A

you can’t tell, benign pheochromocytomas can invade vasculature - would need evidence of metastasis to confirm malignancy

159
Q

explain MIBG scintigraphy

A

inject radio labeled catecholamine precursors and image the person - in a pheochromocytoma you would see an accumulation of these labeled precursors in the area of the tumor

160
Q

patient presents with hypertension, wt loss, headache, hyperglycemia, and sweating - diagnosis? what is unique about the onset of symptoms?

A

pheochromocytoma

5 H’s: HTN, hyper-metabolism, headache, hyperhydrosis, hyperglycemia

onset of symptoms is episodic

161
Q

what is produced in pheochromocytomas?

A

mostly epi and NE, little dopamine (rarely)

162
Q

5 year old presents with tumor in his adrenal gland - give 2 differentials and how would you tell them apart?

A

neuroblastoma (major product is dopamine)
one of the 10% of pheochromocytomas that presents in childhood (produces epi and NE)

to differentiate, look at breakdown products in urine:
if neurblastoma: elevated homovanillic acid HVA (dopamine metabolite)
if pheochromocytoma: elevated Vanillyl mandelic acid VMA (epi and NE metabolite)

163
Q

what are the 3 tumors associated with MEN1? what gene is mutated? association?

A

pituitary gland, parathyroid and pancreas
MEN1 gene
Zollinger-Ellison syndrome (peptic ulcers)

164
Q

patient presents with high cortisol levels that are suppressed with low dose dexamethasone - diagnosis? causes?

A

pseudocushing’s syndrome

chronic stress, anorexia, chronic alcoholism, diabetes mellitus

165
Q

Nests of polygonal spindle shaped cells surrounded by thin vascular stroma - pleomorphism and capsular invasion - diagnosis?

A

pheochromocytoma

166
Q

66 year old lady fainted while grocery shopping. Her labs shows slightly elevated urea and calcium, elevated ALP, and slightly decreased phosphate - diagnosis?

A

hyperparathyroidism

167
Q

what are hydroxyapatite crystals and where do you find them?

A

its the storage form of calcium in bone

168
Q

name 3 ways PTH can regulate serum calcium and phosphate

A
  1. increases bone osteoclast activity (releases calcium and phosphate
  2. increases small intestinal absorption of calcium and phosphate (via activation of vit D)
  3. increases renal calcium reabsorption and decreases phosphate reabsorption (to balance out the gain of phosphate from the first 2)
169
Q

1% of calcium is found extracellulary, name two functions of extracellular calcium

A

neuromuscular excitability

co-factor for clotting enzymes

170
Q

only half of serum calcium is physiologically active, why?

A

other half is bound to albumin

171
Q

what is the active form of calcium in blood? how does pH affect this?

A

active form is ionized calcium which is increased in acidosis and decreased in alkalosis

172
Q

what is 1,25-dihydroxycholecalciferol? what does it do?

A

activated vit D

enhances absorption of calcium in gut and aids in bone resorption to release calcium

173
Q

give the two main causes of hypercalcemia (95%)

A

hyperparathyroidism

malignancy

174
Q

patient presents with hypercalcemia and normal levels of PTH - should you be concerned? what is one cause of this presentation?

A

yes, a patient with hypercalcemia should have low PTH - this is usually caused by an adenoma, but can be a carcinoma or hyperplasia

175
Q

patient presents with polyuria, constipation, peptic ulcer disease, and acute pancreatitis - diagnosis? treatment?

A

hyperparathyroidism

remove affected gland (usually only 1)

176
Q

what condition can cause total plasma calcium to be low, but ionized calcium to be normal?

A

hypoalbuminemia

177
Q

explain the pathogenesis behind chronic renal failure leading to secondary hyperparathyroidism

A

renal insufficiency leads to decreased phosphate excretion. Increased serum phosphate binds free calcium. Decreased free serum calcium stimulates all four parathyroid glands -> bone resorption

178
Q

child is born with a cleft palate, recurrent infections, and tetralogy of fallot - what do you expect his serum calcium levels to be? why?

A

low - he likely has Di George syndrome which results in hypoparathyroidism do to failure of the 3 and 4th pharyngeal pouches to form correctly (where the parathyroid glands develop from)

179
Q

patient presents with numbness and tingling around the lips. Upon attempting to take their BP you notice muscle spasms - diagnosis?

A

hypoparathyroidism

180
Q

patient presents with cataracts, mental retardation, psychosis, seizures and papilledema - diagnosis?

A

prolonged hypocalcemia

181
Q

male presents with testicular atrophy, short stature, and short fingers and toes. His serum calcium levels are low - diagnosis? what do you expect his PTH levels to be? why is his calcium low?

A

pseudohypoparathyroidism (auto dominant)
PTH levels will be high
calcium is low due to end-organ resistance to PTH

182
Q

30 year old man presents hypophosphatemia - lab work comes back unremarkable. What is the most likely cause?

A

chronic alcoholism

183
Q

patient presents with hemolysis and rhabdomyolysis - this is the most serious complication of what disease? name a secondary complication of this presentation

A

hypophosphatemia

can lead to acute renal failure due to the myoglobin released from the muscle destruction

184
Q

is phosphate predominantly an intra or extracellular ion? why is this important when handling blood samples?

A

intracellular
if blood is left sitting around too long in the lab, phosphate will leak out of the cells and result in falsely elevated phosphate levels

185
Q

what deficiency is common with hypocalcemia and hypokalemia? name some effects of this deficiency

A

hypomagnesemia

tetany, agitation, ataxia, tremors

186
Q

person with renal failure later presents with respiratory paralysis and cardiac arrest - what ion imbalance leads to this presentation?

A

hypermagnesemia

187
Q

name 3 pancreatic endocrine tumors associated with MEN1. What are the other two organs involved with MEN1?

A

gastrinoma, insulinoma, glucagonoma

parathyroid, pituitary

188
Q

give one explanation of why calcium levels might be high, but PTH levels low?

A

tumor secreting PTHrp (PTH related protein) - its a PTH agonist that has all the same functions as PTH

System Path II (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions