Brainscape's Knowledge GenomeTM

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


See full index

IPAP JUNIOR SEM. > Endo Block 1 > Flashcards

Endo Block 1 Flashcards

1
Q

For endocrine homones what are the biological active fraction, bound or unbound

A

Unbound (free)

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

What are the two basic classes of hormones

A

polypeptides (proteins) and steroids (thyronines)

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

How are steroids chaparoned thoughout the body

A

By binding to a protein

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

High levels of circulating hormone produces what in negative feedback

A

Decreases hormone synthesis and secretion

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

Low levels of circulating hormone has what response in negative feedback loops

A

Increase hormone synthesis

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

In hyperfunction of endocrine tissue what is primary disfunction

A

Alteration of the hormone secreting gland

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

In hyperfunction in endocrine tissue what is secondary disfunction

A

Alteration in pituitary or hypothalumus

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

What is ectopic endocrine tissue disfunction

A

Hormone secreted from tissue other tahn usual sourse

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

What is resistnce endocrice disfunction

A

Inability of target tissue to recognize the hormone

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

What is an adenoma

A

Adenoma—benign enlargement of a cluster of glandular (secreting) cells
Can become malignant (i.e. adenocarcinoma)

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

What is a neoplasm

A

Neoplasm—abnormal new growth of tissue

Generally considered malignant

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

What is hyperplasia

A

Hyperplasia—benign enlargement of entire gland

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

What is the differnce between atrophy and hypoplasia

A

Atrophy – the wasting away of existing cells

Hypoplasia – underdevelopment or incomplete development (congenital)

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

What is the single best screening lab for someone with hypothyroidism

A

Screen the pituitary ( TSH)

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

What are the two hormones secreted from the posterior pituitary gland

A

Oxytocin and ADH

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

Is the post pituitary a gland

A

Not a gland but is the distal axon terminals of the hypothalamic neurons

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

What are the two receptors for ADH

A

V1 and V2

V1 receptors are found in blood vessels, constricts vascular smooth muscle (however it is a weak pressor)

V2 receptors are found in the collecting duct of the kidney, and they cause water to be retained in the body

The major function of ADH is to retain water in the body

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

What is the major function of ADH

A

NO PEEING, to retain water in the body

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

What is the response of ADH to osmolarity increases

A

ADH is released

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

Where are the V2 receptos for ADH

A

Works in the collecting tubel and increases aquaporins to increase water absorption

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

What are the two regulators for ADH secterion

A 
#1 - Osmoreceptors in hypothalamus
-1% INCREASE in plasma osmolality releases ADH 
#2 - Baroreceptors in arteries and atria
-10% or greater DECREASE in plasma volume or pressure, releases ADH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What effect does alcohol have on ADH secretion

A

Inhibits ADH and increase urine output

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

What is SIADH

A

Too much ADH, SI makes you SWELL! Retain fluid

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

What is Diabetes insipidus

A

Not enough ADH, DI makes you DRY, PEE OUT ALL YOUR FLUID

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

What are the initial clues of SIADH

A

normal or expanded plasma volume, but NOT low plasma volume

low serum sodium (hyponatremia)

high urine specific gravity (SG)

high urine sodium

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

What are the top three causes of SIADH

A

Central nervous system or lung disorders

Malignancy - tumors which secrete ectopic ADH

Prescription and recreational drugs

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

80 percent of lung tumors associated with SIADH are..

A

Small cell lung cancer

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

A pt presents with unexplained hyponatremia and oliguria/ anuria…
What should you order

A

Chest Ct or MRI r/o malignancy

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

What effect does antineoplastic medication have on ADH

A

Increased secretion (SIADH) due to nausea mechanism

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

What effects for NSAIDs have on ADH

A

Increase ADH by inhibiting prostaglandins

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

What medications induce SAIDH

A

Antidepressants ( SSRI, TCA, MAOI)
Anti neoplastic agents ( that cause nausea)

MDMA- Exctasy
NSAIDs
Opiates

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

Low Na+ in the setting of SIADH is due to…

A

Excess water, not lack of sodium

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

What are the early S/s of low serum Na+

A

Fatigue
HA
Nausea

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

What are late signs of Low serum Na+

A

Letharfy, confusion, stupro, and coma

Neuromuscular excitabilty, muscle twitching a SZR, from electrolyte abnomrl

Vomiting and abdominal cramps

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

What are the labs values in SIADH

A

Low plasma osmololity
W/ normal plama volume

HypoNa+ (<135)
High urine osmololity compared to plasma (>20mEq/dL)

Low BUN (<10 mg/dL) 
Hypouricemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the Tx approach to euvolemic, aS/s or mild S/s of SIADH

A

Water restriction

Demeclocycline ( if the pt cant adhere to water restriction)

Ensure adequate dietary Na+ intake

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

What is the Tx appraoch to S/s and severe hyponatremia

A

Raise serum Na+ by o.5-1 mEq/ hr to a max 125-130 (avoid locked in syndorme) No more than 8-10 mmol in a 24 hour period

3% hypertonic saline– for emergencies only (CNS symptoms present)
-Seizures, confusion, etc.

Furosemide—increases free H2O excretion

Tolvaptan (V2 receptor antagonist) – mediates the diuretic effect of ADH

These medications would be used in consultation with a nephrologist

Monitor serum sodium levels frequently (q 1-2 hours)

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

What is the referral criteria for SIADH

A

Nephrology or Endocrinology referral for SEVERE, uncertain, refractory, or complicated cases

If AGGRESIVE therapies are needed, such as with hypertonic saline, demeclocycline, V2 receptor antagonists, or dialysis

In patients with end liver or heart disease

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

A pt presents with 2-20 L of urine production in 24 hours think

A

Diabetes insipidus

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

What is a normal urine osmolality

A

300 mOsm/kg

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

What are the 4 main types of DI

A

Central (important)

Nephrogenic (important)

Primary Polydipsia

Gestational

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

What causes nephrogenic DI

A

Decreased ability to concentrate the urine due to resestance to ADH in the kidney

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

What is sheehan syndrome

A

Massive blood loss post parturm, leading to hypovolemic shock and pituitary infarction ( may cause DI)

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

What are the common causes of Nephrogenic DI

A

Medications like LITHIUM, demeclocycline, ETOH, CAFFINE, Wt loss medicaions

Hypokalemia and hypercalcemia

Renal Dz

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

A pt presents with polydispsia, polyuria with a normal serum sodium, (with possible nocturia)

Think ?

A

Classic presentation of DI

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

How does an unconscious pt present with DI

A

HOTN, vascular collapse, Hypernatremia

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

What is a urine output volume that would r/o DI

A

Less than 2L in 24 hrs

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

What is a vasopressin challange test

A

A w/u for central DI Dx

Patient is admitted to hospital
-Give desmopressin acetate (0.05-0.1 mL/1mcg)*intranasally, subcutaneously or intravenously

Measure urine volume before for 12 hrs, then after DDAVP

Measure serum sodium at baseline, 12 hours after DDAVP

If pt has Central DI, they will have decreased thirst, decreased urine output, increased urine osmolality

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

A pt with an elevated ADH during fluid restriction

Think

A

DI

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

What is the Tx approach to Central DI

A

DDAVP, lowest effective dose 2-3 x a day

Monitor elecrtrolytes

Avoid dehydration ( V/D)

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

What is the tx appraoch to Nephrogenic DI

A

Indomethacin 50 mg q 8hrs

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

What is the adenohypophysis

A

The anterior pituitary

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

What is the relationship with ACTH and MSH

A

ACTH stimulates alpha-MSH in the Ant. Pituitary

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

What is the effect of pregnancy on the Ant. Pituitary

A

Doubles in size

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

What is the diff between clinically functioning and non functioning pit. Adenomas

A

Functioning is secreting at least 1 hormone, non functioning is not and typically found on accident

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

What is the diff between macro and micro adenomas

A

Macro : >1 cm and micros are less

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

What is the procedure of choice to investigate a pituitary problem

A

MRI!

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

What effect does dopamine agonists and somatostatin have on Prolactin secrtion

A

Decrease/ Block the secretion

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

What is bromocriptine

A

A dopamine agonist that can suppress the secretioin of Prolactin

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

What is a normal prolactin level

A

Less than 20mg/dl is normal

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

What effect does glucose have on Growth Hormone

A

Hyper glycemia suppresses Growth Hormon secretioin, Hypoglycemia stimulates Growth Hormone production

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

What is the Tx of choice for Acromegaly

A

Transsphenoidal resection (SRGRY)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What cardiac conditions are assoc. with acromegaly

A

Valvular regurgitation and persistant HTN

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

What is cushings “disease”

A

A cortisol hormone d/o that comes from the brain ( secondary)

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

What is cushings “syndrome”

A

Primary adrenal problem with cortisol

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

What is the most common cause of cushings syndrome

A

Taking too much corticosteroids

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

A pt presents with central obesity, facial plethora, thin skin with easy bruising, proximal muscle weakness, HTN and DM

Think?

A

Hypercortisolism ( adrenal, ACTH problems)

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

What is the test to assess corticotropic adenomas

A

A dexamethasone supression challange

and a 24 hour urine

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

What is the Tx of choice for a Cushings Disease

A

Surgical removal of the tumor

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

A pt presents with sudden severe headache, AMS, Vomitting, Ocular defects, with HOTN

Think

A

Pituitary D/o likely hypo

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

In hypopituitary d/o what are the order of loss hormones

A

GH is lost first

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

What are the common S/s of hypothroidism

A

Fatigue, letharfy, constipation , depression, wt gain, cold intolerance, dyspnea on execrtion, menorraghia, arthlagias, parasethisias

(Metabolism is down)

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

How with DTRs present with hypothyroidism

A

Delayed relaxation

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

What is the single best test to evaluate hypothyroidism

A

TSH

May be increased/ elevated in primary
And may be low in secondary

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

What is a normal TSH level

A

0.4-4.0 mL/L

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

When should TSH be checked after starting levothyroxine tx

A

Not until after 6 weeks!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

How should levothyroxine for hypothyroidism be taken

A

Must take in the AM, without other food or drugs,

At least 4 hours before other drugs

LONG TERM!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the dosing regiment for levothyroxine

A

Start at 50 mcg/ day then increase q 6 weeks by 25-50 mcgs until target dose is reached

(1.6 mcg/kg/day)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is the TSH goal for hypothyroidism Tx

A

A TSH between 04.-2.0 mL/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What effect does pregnancy have on Levothyroxine Tx

A

Dosage requires in the 5th week of pregnancy a 20-30% increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

A pt with hypothyrdoidism + hypercapnia, + myxedema coma… what do you do

A

ADMIT!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is cretinism

A

Congenital hypothyroidism

Hypoplastic or failure of the thyroid to migrate to its appropriate location

Usually heriditary from hashimotos

S/s: slow mentation, slow bone development, decreased longitudinal growth, Thick dry scalp, with delayed sexual maturation

Tx: levothyroxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Resting tremor is a sign and symptom of what D/o

A

Hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How does Graves Dz present

A

High Thyroid s/s
Bruit + enlarged thyroid
Non pitting edema
SubQ infitrates

Exopthalmos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is thyroid acopathy

A

Swelling/ clubbing of the fingers seen in graves dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

A pt presents with LOW TSH and High T3 T4 think

A

Hyperthyroidism, Graves Dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are the Tx approachs to Hyperthyroidism

A

Methimazole

Proprothyuricil ( pregnant seeking pts)

Surgery

S/s control with b blockers
radioactive therpay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are the ADE of Tx of hyperthyroidism

A

Rash, agranulocytosis, N/ dyspepsia, Liver failure with PTU 1:1000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What are Orargrafin and telepaque

A

Bridge therapy to surgery for hyperthyroidism

Used for severe S/s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is the Tx of Choice for Graves Dz (Hyperthyroidism)

A

Ablation of the thyroid with radiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is the Tx appraoch to exopthalmos

A

Corticosteroids (treat during the ablation of the thyroid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What are the three indications for surgery of the thyroid in hyperthyroidism

A

Large obstructive gland, risk of malignancy, or pregnant women with uncontrolled S/s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the most common type of thyroid cancer

A

Papillary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is the most aggresive form of thyroid cancer

A

Anaplastic

Which is also the least common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What is the most sig RSK fx for development of papillary thyroid cancer

A

Exposure to radiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is the Tx of choice for Thyroid Cancer

A

SURGERY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Post surgical RAI is only effective on what two types of thyroid cancer

A

Papillary and follicular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What is the tx approach to thyroid storm

A

Admit to ICU
+propranolol
+ Proprylthiuricil
+ Corticosteroids

B Blockers can be used for cardiac S/s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is the Tx approach to myxedma coma

A

IV levothyroxime

Supportive care, passive warming, electrolyte correction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Where does ACTH have its action in the adrenal gland

A

Reticularis and Fasciculata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is ACTH made from

A

Pituitary corticotropes

102
Q

What is the pattern of secretion with ACTH

A

Diurnal rhythm
Earlest at 0400

Lowest at night

103
Q

What is the most common ACTH producing tumor

A

Small cell lung tumor

104
Q

What is the testing approach to Cushing syndrome Dx

A
  1. Dexamethasone Test (Tests ACTH)
    (If elevated in the AM then think Cushing syndrome)
  2. 24 hours urinary free cortisol test
    (Confirms if cortisol is high or not)
  3. Check a baseline ACTH
    (If NML or elevated= get an MRI) (Cushing Dz)
    (If VERY VERY elevated= get a Chest CT )
    (Ectopic ACTH Secretion)
105
Q

What is the most common cause of adrenal insufficiency

A

Autoimmune adrenalitis

Also TB

106
Q

What is the Test approach to Addisons Dz

A

1st: check serum cortisol
2: sythetic ACTH test

3: no response= Primary
Responce= secondary

107
Q

TRH stimulates what two hormones

A

TSH and PRL

108
Q

PRL inhibits what hormone

A

LH

109
Q

GHinhibiting Hormone inhibits what two hormones

A

TSH and GH

110
Q

What is another name for dopamine

A

Prolactin inhibiting hormone

111
Q

What effect does cabergoline, bromocriptine, and pergolide have on PRL

A

Decreased secretion of PRL

112
Q

What effect does hypothyroidism have on PRL

A

Increased secretion of TRSH which increases TSH and PRL

113
Q

What is the Tx of choice for prolactinomas

A

Levothyroxine if hypothyroidism

Dopamine agonists: Cabergoline (pregnant pts)
or bromocriptine

Can D/c Tx after 24 months

114
Q

What inhibits GH

A

GHIH, Hyper glycemia, Hypothyroid, Glucocorticoids,

IGF1

115
Q

What is the DDX of gigantism and acromegaly

A

Gigantism is GH oversecrtion in a child Acromegaly is oversecretion in adults

116
Q

What is the Dx approach to acromegaly

A

Random IGF1 level, If abnormal then obtain a fasting IGF1 level, then give 100 mg glucoes, then measure IGF1 again, if GH is greater than 1mcg/L then confrimed

117
Q

Prolactin level high? Investigate…

A

Prolactinoma OR GH tumor

118
Q

What is the FU criteria for acroegaly

A

At least annual IGF1
Cardiac followup for valvular dz
Or HTN

119
Q

A pt presents with sudden severe HA, altered LOC +wkness, Vomiting and ocular defects +HOTN

Suspect

A

Infarction/ pituitary apoplexy

TX w/ glucocorticoids follwed by surgery

120
Q

What is the most commonly affected endocrine structure in head truama

A

Ant pit

121
Q

What are the recommended screening labs in head truama

A

Recommended screening labs include: 0800 cortisol, TSH, T4, LH, FSH, IGF-1, testosterone (males), estradiol (females)

122
Q

What is the order of loss in pituitary failure

A

Gradual loss of normal pituitary function.
In order of loss: GH, gonadotropins, TSH, ACTH
PRL deficiency is rare

123
Q

A pt presents with increased abdominal adipose tissue, decreases streghnt and excercise capacity, decrease in total lean body mass, elevated SBP, increased LDLs

Think what hormone deficiency

A

GH

124
Q

A pt presents

Girls: delayed breast development, scant pubic/axillary hair, primary amenorrhea

Boys: small phallus & testes, sparse body hair

Adult females: breast atrophy, loss of pubic/axillary hair, secondary amenorrhea, infertility

Adult males: testicular atrophy, decreased libido, loss of body/facial hair, ED, infertility

Think what hormone deficiency

A

LH/FSH

125
Q

A pt presents with weakness, fatigue, wt gain, constipation, cold intolerance, and a slow HR

Think what hormone deficiency

A

TSH

126
Q

How will labs present in hypopituiary

A

Both pituitary and targert hormones will be low

127
Q

What two mechanisms increase aldosterone secretion

A

Angiotensis II and Hyper K

128
Q

What is the main cause of refractory HTN

A

Hyperaldosteronism

129
Q

What is conn syndrome

A

Unlilateral aldosterone secreting adrenal adenoma

Mc in women

130
Q

Bilateral adrenal hyperplasia is most common in men or women?

A

Men

131
Q

What are the three main causes of hyperaldosteronism

A

Unilateral aldosterone-producing adrenal adenoma (Conn syndrome)
Women MC

Bilateral adrenal hyperplasia
Men MC

Aldosterone producing adrenocortical carcinomas

132
Q

What is the most common cause of excess renin production

A

Renal artery stenosis

133
Q

What is the most common cause of adrenal insufficiency

A

Abrupt stop of steroid use

WE CAUSE THIS

134
Q

A pt with diastolic hypertension is a key finding of what D/o

A

Hyperaldosteronism

135
Q

What is the Dx criteria for hyperaldosteronism

A

Sustained HTN 150/100
(3 diff days)

HTN resistant to 3 anti-HTN drugs

Controlled BP needing 4+ drugs

Hypokalemia

Personal/family hx of early-onset HTN or CVA aged <40

1 degree relative with primary aldosteronism

Presence of an adrenal mass

Low plasmin renin activity (PRA)

136
Q

A pt that has HTN and hypokaleia

Think

A

Hyperaldosteronism

137
Q

What are the steps to ordering a plasma renin activity

A

1st correct the hypokalemia
Next eat a ton of salt
(more tha 6g)

Stop diuretics, ace, Arbs , BB, Nsaids, and OCPS

Then draw when pt OOB x 2hrs between 8-10 am

Also order a K+ level and an aldosterone level

138
Q

When ordering a PRA (renin), a suppressed PRA means…

A

Primary hyperaldosteronism

139
Q

When ordering a PRA (renin), what does an increased PRA mean…

A

Secondary hyperaldosteronism

Due to renal artery stenosis
Leading to increasaed aldosteronism

140
Q

What is the DX approach to hyperaldosteronism

A

24 hr aldosterone level,

(Primary presents with elevated aldosterone)

Then order a CT or MRI to r/o adrenocortical carcinoma (MC in women) or a adrenal hyperplasia (MC in Men)

141
Q

What is the Tx apprach to Conn Dz

A

Conn Syndrome is an adenoma

Tx: surgery

142
Q

What is the Tx approach to bilateral adrenal hyperplasia

A

TX: Spironolactone (Aldactone) - K+ sparing diuretic and aldosterone antagonist
OR
Eplerenone – K+ sparing diuretic favored in pregnancy and for men
(pregnant women cant get spirals)

143
Q

What is the Tx approach to renal artery stenosis

A

Angioplasty or revasc procedures

Referral to cards

144
Q

What is congenital adrenal hyperplasia

A

A subset of primary adrenal insufficiency – due to defective cortisol synthesis

145
Q

What enzyme is required for cortisol synthesis

A

21-hydroxylase is an enzyme required for cortisol synthesis

146
Q

What are the two main types of Congenital adrenal hyperplasia

A

Classic Vs non classic

Classic CAH – “salt-wasting”
Severe enzyme deficiency (0%-2%)
Present in utero and at birth
Deficiency in cortisol and aldosterone
Excess androgens (progesterone and 17-hydroxyprogesterone)
Both are aldosterone antagonists and cause hyperkalemia and hyponatremia, dehydration

Non-classic CAH:
Milder enzyme deficiency (20%-50%)
Presents after adrenarche (6-7 yo)
Most frequent autosomal recessive disorder in humans (Yupik Alaskans, Ashkenazi Jews, Natives of La Reunion Island)

147
Q

What are the S/s of classic “salt wasting” Congenital adrenal hyperplasia

A

S/S of Classic CAH:

  • Death of fetus or infant
  • Masculinization of external genitalia in female infants
  • Precocious sexual development of male infants
  • Short stature due to premature closure of bone epiphyses
148
Q

What are the S/s of non classic congenital hyperplasia

A 
S/S of Non-Classic CAH:
Late onset (during/after puberty)
Hirsutism and acne are predominant signs in females
HTN
Oligomenorrhea and infertility
149
Q

What is the key lab to Dx congenital adrenal hyperplasia

A

Evaluate 17-hydroxyprogesterone level (precursor to 11-Deoxycortisol; deficiency of 21-hydroxylase leads to excess 17-hydroxyprogesterone)

150
Q

What is the Tx approach to congenital adrenal hyperplasia

A

Treatment:
-Glucocorticoid to suppress ACTH secretion
—Prednisone, cortisol, or dexamethasone

-Replace mineralocorticoids if needed
—Fludrocortisone (Florinef)

  • Spironolactone (Aldactone) may be prescribed – (aldosterone antagonist with anti-androgen activity)
  • Salt supplements
151
Q

What is the MOA of spirinolactone

A

Spironolactone (Aldactone) may be prescribed – (aldosterone antagonist with anti-androgen activity)

152
Q

Where is epi and NE produced

A

In the adrenal medulla

153
Q

What is a pheochromocytoma

A

A freaking UNICORN

Tumor of the adrenal medulla

Secrets Epi and NE

154
Q

What is a paraganglioma

A

Tumor outside the adrenal galnds on a ganglia that either secrets NE or nothing

155
Q

What is the S/s triad of pheochromocytoma

A

Headache, diaphorsesis, and palpatations

156
Q

What drugs trigger pheochromos paroxysms

A

Drugs: MAOIs, caffeine, nicotine, decongestants, amphetamines, cocaine, IV contrast, epinephrine, corticosteroids
General anesthesia

157
Q

What can trigger a HTN crisis or fatal arrhythmia in a pt with pheochromocytoma

A 
IV contrast dye
Glucagon injection
Needle biopsy of the mass
Anesthesia or surgical procedures
Vaginal delivery
158
Q

A pt presents with HTN (either sustained or paroxysmal)
Facial pallor, mottled cyanosis, then flushing, +tachycardia
+/- precordial pain

Can also presetn wtih ARDS, Cardiomyopathy, Liver failure, or Death

A

Pheochromocytoma

159
Q

What is the DX appraoch to pheochromocytoma

A

Order DDX labs: Free T4, TSH, CBC, ESR, gl

Then to r/o pheo:
Order a Plasma fractioned free metanephrines
(If normal= no pheo)

Next step:
Urinary fractioned metanephrines and creatine
(24 hr urine)

postive finding is Labs 3x ULN

Once postive finding order a non con CT or the abdomen and adrenals (Can use abd MRI)
(Contrast can trigger a paroxysm or HTN crisis)

160
Q

What is the most senstive imaging for a pheo

A

68Ga-DOTATOC-PET

161
Q

What is the approach to TX of a pheo

A

Preop Alpha blockade (Phenooxybenzamie)
Or
CCB ( nifedipine)
DO NOT GIVE BB FIRST

Preop: BP must be controlled for 4-7 days prior with ECG monitoring

Inra op: Monitro BP closely
(Nicardapine for HTN crisis)

Post op: urine catecholamines and BP monitoring

If In OP: Metyrosine

162
Q

What is MEN 1

A

Hyper Parathyroid, pancreatic, and pituitary invovlmet
Facial angiofibromas
Enteropancreatic tumors
Adrenal adenomas

Hypercalcemia (1st sign)

PHEO (RARE)

AKA wermer sydrome
(MC)

Tx aimed at removing tumors and controlling hypercalcemia

163
Q

What is MEN 2a

A

Medullary thyroid cancer
PHEOS! BILATERAL
Hyperparathyroidism
HIRSCHSPRING DZ

MEN2a is more rare, and is autosomal dominant
(Siblings and children)

Tx approach is pophylactic thyroidectomy (prevents medually thyroid cancer, but you MUST screen them for a PHEO 1st)

164
Q

What is MEN 3 (2b)

A 
Mucosal and GI neuromas 
Meduallry thyroid cancer 
PHEOs! 
SKELETAL ABNMLS ( MARFANS) 
Delayed puberity

Tx: early prophylactic thyroid removal ( prevents medullary CA)

165
Q

What is MEN4

A

Parathyroid adenomas (80%)
Pancreatic neuroendocrine tumors
Pituitary adenoma
Adrenal tumors

Alos prone to renal tumors, test CA, cercival CA, and primary ovarian failure

4 effects the gonads

166
Q

What is the appraoch to finding an incedental adrenal mass

A

Order
Plasma fractioned free metanephrines (PHEO)
Order ACTH and serum cortisol ( Cushings or addisons)(if abnml order a dexamathasone suppresss test)
Order a PRA (renin) and aldosterone level

Then serial CT scans a 6 and 12 months (determine if its nonfunctional or less than 4 cm)

Then CT every 2-3 years if the mass is static in growth

ALERT-
If the mass is greater than 4 cm, it should be surgically remover and biopsied even if its non functional

167
Q

What are the red flags for secondary HTN in endocrine HTN

A

Hypokalemia without diuretic Rx

Presentation at an early age without a family history of HTN

New presentation of HTN in patients > 50 years old

Higher degree of severity
Diastolic > 110mmHg

Well controlled HTN that is suddenlt refractry

Increased BP which is paroxysmal (PHEO!)

HTN without obestiy

OR
New S?s suggestive of a endocrice D/o

168
Q

What does a meduallry thyroid cancer secrete

A

Calcitonin, prostaglandins, serotonin, ACTH, corticotropin-releasing hormone

Think of this in a pt with MEN 2a

169
Q

What are the drugs that specifically stimulate ADH secretion

A

SSRIs, TCAs, MDMA, NSAIDs, Amioderone, Antipsycotics

170
Q

What is the relationship between TRH and PRL and TSH

A

Thyroid releasing hormone stimulates not only TSH but also PRL

171
Q

PRL inhibits what hormones

A

LH

172
Q

GHIH inhibits not only GH but what other hormone

A

TSH

173
Q

What are the two ost common pituitary adenomas

A

PRL secreting and GH secreting

174
Q

Any pt that presents with visual field defects,,, you must investigate

A

R/o a pituitaty/ hypothalamic mass

175
Q

The first line therapy for ademnomas is _______, except for ______ which is med Tx first

A

Surgery, except for PRL adenomas with are treated with surgery

176
Q

How is prolactin secreted differnetly than other hormones

A

Secreted continuosly unless inhibited by dopamine

177
Q

What effect does hypothyroidism have on PRL

A

Hypothyroidism (Thyrotropin releasing hormone (TRH) is the precursor to TSH in the anterior pituitary that can stimulate PRL)

178
Q

GH secreting adenomas often secrete what other hormone

A

PRL

179
Q

What effect does hypothyroidism have on growth hormone

A

Inhibtis its secretion

180
Q

What is the manner in which GH is secreted

A

Pulsatile anner, 8-12 pulses in a 24 hr period

181
Q

What is the major secretory product of the thyroid

A

T4

182
Q

How will T4 be in hypothyroidism vs hyperthroidism

A

Will be Low in hypo, High in hyper

183
Q

How will T3 be in thyrotoxicosis

A

Will be high in thyrotoxicosis
(better test for diagnosis than free T4)

Not accurate for diagnosing hypothyroidism due to increase in relative secretion of T3 in hypothyroidism

184
Q

What test Dx for hashimotos

A

Anti-TPO

But can also be seen in Graves Dz

185
Q

What tests are specif to Dx graves Dz

A

Anti-thyrotropin receptor antibodies (i.e. anti-TSH receptor, or TSH receptor stimulating antibody)

186
Q

What imaging study should be ordered for pts with S/s of thyrotoxicosis

A

RAIU scan

187
Q

What is the indication for a RAIU scan

A

For patients with s/s of thyrotoxicosis

To determine quantity of radioiodine txt for hyperthyroidism

For evaluation of a suspicious nodule

To evaluate metastatic thyroid cancer

Identify if a mass is ectopic thyroid tissue

188
Q

What is the bst method for differentiating benign from malignant thyroid nodules and diffuse goiters

A

Fine needle Aspiration BIOPSY

189
Q

What is the Tx approach to painful subacute thyroiditis

A

ASA, prednisone x 2 wks, BB (propranolol), +levo if hypothyroid

Remember, this usually resolves completely and spontaneously over weeks to months

190
Q

What is the most common type of thyroiditis

A

Hashimoto

chronic autoimmune dz

191
Q

What is the hallmark lab in Hashimoto (chronic) thyroiditis

A

AntiTPO

FT4 initially high, then low

192
Q

What types of thyroiditis present with pain and which do not

A

Infectious, riedels, and dequervains present with pain

Chronic/ Hashimoto and post partum do not

193
Q

A pt presents with HX of VRI, painful goiter/ thyroid, low grade fever, and dysphagia…

Think

A

Dequervains thyroiditis (painful)

194
Q

A pt presetns with a previous strep throat infx, fvr, sever pain and erythamatous thyroid…

Think

A

Infectious thyroiditis

195
Q

A pt presents with slowly enlarging stony mass within the thyroid
Think..

A

IgG4 related (riedel) thyroiditis

196
Q

What is the Tx appraoach for Riedels thyroidittis ( stony mass)

A

Surgery, +tamoxifen (may cause remession)

+corticosteroids

197
Q

What is the Tx appraoch to a Bening multinodular goiter that presents with an elevated TSH level

A

If TSH is elevated, may treat with levothyroxine to suppress TSH level and achieve euthyroid state

198
Q

What is the most common cause of hypothyroidism

A

Hashimoto thyroiditis

199
Q

What are the cholesterol and prolactin levels in a pt with hypothyroidism

A

Elevated in both

200
Q

What is myxedmea madness

A

Orgnanic psychosis with paraboid delusions seen in hypothyroidism

201
Q

A pt with hypothyroidism and signifigant CAD needing levo tx

What do you do

A

REFER!

202
Q

What is the differnce between cretenism and childhood hypothyroidism

A

Cretenism is present at birth, child appears normal then does not develop appropriately

Childhood hypothyroidism presents later in development, near puberty, pt does not sexually mature appropriately

203
Q

What are some complications of exopthalmos associated with graves dz

A

Inflammation of eye muscles due to lymphocyte infiltration

Proptosis

Periorbital edema

Diplopia

Optic nerve compression

Blindness

204
Q

On xray you see periostitis phalanges and metacarpals

Think

A

Thyroid acropachy in graves dz

205
Q

What is the MOA od methimazole

A

Inhibits production of T4

Used to treat hyperthyroidism/ Graves

206
Q

What is the MOA of propythiouracil

A

Inhibits production of T4 and blocks conversion of T4 to T3

Used if the pt wants to get pregnant

207
Q

WHat are the common complications of Graves Dz trreatemnt

A

Rash (exfoliative dermatitis)

Agranulocytosis (1/1000) - monitor w/ CBC

Nausea/dyspepsia

Liver failure with PTU 1:1000

208
Q

What is a tx option for pts with severe graves dz as a bridge to surgery

A

Oragrafin or telepaque ( Iodinated contrast agents)

Temoporary tx

Blocks T4 to T3 conversion

209
Q

What is the pt education required for a Thyroid ablation with I131

A

Contraindicated in pregnant or
lactating mothers

Contraception recommended for
women AND MEN for 6 months following
RAI treatment

210
Q

If a pt has exopthalmos can they get radiation ablation

A

Ehhhhh its a relative contra

Worse in smoking pts

211
Q

What is apathetic hyperthyroidism

A

A subtle presentation of graves in an older pt

Weight loss
Fatigue
Lethargy
Depression
Consider this in elderly patients with new mood disorder
May also present with angina pectoris
212
Q

A older pt presents with new mood d/o and angina pectoris

Think

A

Apathetic hyperthyroidism

213
Q

A pt with a serum elevated calcitonin … think

A

Thyroid nodule/ cancer

214
Q

A firm thyroid nodule greated than 4.5 cm think

A

Cancer

215
Q

Do pure cyctic nodules require FNAB

A

No

216
Q

What is the Tx approach to thyroid nodules

A

Benign: serial US, FNA if increasing in size

If TSH is elevated/ Hypothyroidthen Levo

SRGY: suspicious nodules

RAI TX fro pts with hyperthyroid, toxic thyroid, MNG, or Graves

217
Q

Where does follicular thyroid cancer often metz to

A

Neck lymph nodes, bones and lungs

218
Q

What types of thyroid cancer do not absorb iodine

A

Medullary and anaplastic

219
Q

What type of thryoid cancer is assoicated with MEN2a and 2b

A

Medullary

220
Q

Medullary thyroid cancer secretes what hormones

A

Calcitonin, prostaglandins, serotonin, ACTH, corticotropin-releasing hormone

Useful in symptom recognition and monitoring (flushing, diarrhea*)

221
Q

What does a follicular carcinoma secrete

A

FT4 can lead to hyperthyroidism

222
Q

What lab can tell you if the pappilalry or follicular carcinoma is metastatic

A

Thyroglobulin

223
Q

Amioderone is the cause of 20% of what emergent thyroid condition

A

Thyroid storm

224
Q

What is myxedema

A

Fluid retention from hypothyroidism

225
Q

A pt presents with severe AMS, convulsions, severe hypothermia, bradypnea, hypo Na+, hypo gl, HOTN

Think

A

Myxedema crisis

226
Q

What medication must be avoided in myxedmea crisis

A

OPIODS!

227
Q

ACTH stimualtes what 3 pathways

A

Cortisol production, aldosterone sectreion, melanin production

228
Q

What are 4 effects of excess cortisol

A

Inflammation is suppressed
Immune suppresion
Osteoporsis
Weight gain

229
Q

A pt presents with weeakness and fatigue, salt cravings, amenorrhea, otho HOTN, N/V, FEVER, hyperpigmentation, and hyperkalemia, +/- met acidosis

Think

A

Addisons

Draw a plasma ortisol level (will be low at 8 am) followed by an ACTH level (will be high)

Confirm with a cosyntroprin stimuation test

230
Q

What is the Tx approach to primary addisons

A

Replace steroids levels with hydrocortisone or prednisone
+/- fludrocortisone for sodium retention

Needs 2x sick day dosing

Emergency steroid kit of 100mg hydrocortisone

Must wear medical bracelet

231
Q

What is the Tx appraoch to secondary adrenal insufficiency

A

Replace steroid levels with cortisone, dexamethasone, or prednisone

No need to use fludrocortisone

Tx underlying pituitary d/o

Needs sick day dosing and wear of medical bracelet

232
Q

What RSI medication can cause adrenal crisis

A

Etomidate

233
Q

A pt presents with extreme weakness, HOTN, fever, N/v dehydration, hypoglycemia!,. Headache and AMS

Think

A

Adrenal crisis

234
Q

What is the hallmark feature of adrenal crisis

A

Hypoglycemia

235
Q

What is the Tdx approach to adrenal crisis

A

Immediate cortisol level (low)
Treat with steroids

Next- cosyntropin test ( will be low)

Admin high dose steroids with broad spec abx

236
Q

What is the net electrolye efect of aldosterone

A

Holds onto sodium in exchange for potassium

237
Q

Renal artery stenosis stimulates the release of what hormone

A

Aldosterone

238
Q

What is the most common cause o excess renin secretrion

A

Renal artery stenosis

239
Q

What are the 3 main etiologies of hyperaldosteronism

A

Unilateral adrenal adenoma (COnns)

Bilateral hyoperplasia (MC men)

Carincomas

240
Q

What are the s/s of hypo K+

A

Muscle weakness, paresthias with tetany
HA
Polyuria polydipsia

241
Q

How do you order a PRA for hyperaldosteronism

A

1st correct they hypo K+
Then eat 6g of salt
Stop any diuretic medications

Draw PRA when pt OOB x 2 hrs between 8-10 am

If PRA is suppresed its primary hyperaldosteronism

If PRA is increased or normal its seccondary 2/2 renal artery stenosis

242
Q

A pt with an elevatede PRA after 6g ingestion fo salt is a sign of

A

Renal artery stenosis (2ndary hyperaldosteronism )

243
Q

WHat is the Dx appraoch to hyperaldosteronism

A

It will be a pt with a high diasotolic BP and hypokalemia

1) correct hypok+
2) eat 6g of salt
3) stop diuretics
4) draw PRA with pt OOB x 2 hrs between 8-10 am
5) if PRA is suppresed its primary
6) if PRA is NML or elevated its secondary due to renal artery stenosis
7) order 24 hr urine ( primary will have levated aldosterone)
8) order ABD CT or MRI to r/o carcinoma or hyperplasia

244
Q

What is the Tx for unilateral adenomas (Conns)

A

Surgery removal

245
Q

What is the Tx for bilateral adrenal hyperplasia

A

Spirnolocatone

Or eplererone if pregnant or in men

246
Q

What is the tx for renal artery stenosis

A

Angioplasty or revasc

247
Q

What part of the nervous system do the adrenal gland and the ganglia belong to

A

Autonomic/ Sympathetic

248
Q

What medications can trigger a paroxyms

A

MAOis caffine, nicotine, decongestants, cocaine, meth, IV contrast, Epi, steroids, general anesthestia

249
Q

What are the inoperative options for pheos

A

Metyrosine

250
Q

How long should BP be controlled prior to pheo surgery

A

4-7 days prior

251
Q

How is BP controlled during a pheo surgery

A

IV nicardipine for any HTN crisis

252
Q

What is the size determination that a pheo is metz

A

Bigger than 7 cm

IPAP JUNIOR SEM. (43 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions