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UWorld - Endocrine > Path / Pathophys > Flashcards

Path / Pathophys Flashcards

1
Q

Famililal Chylomicronemia Syndrome

(Type 1 Familial Dyslipidemia)

  1. What protein is defected?
  2. What lipoprotein is elevated?
  3. What are the major clinical features?
A
  1. Lipoprotein Lipase + Apolipoprotein C-II
  2. Chylomicrons

3.

  • acute pancreatitis
  • lipemia retinalis (milky plasma)
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2
Q

Famililal Hypercholesterolnemia Syndrome

(Type 2 Familial Dyslipidemia)

  1. What protein is defected?
  2. What lipoprotein is elevated?
  3. What are the major clinical features?
A
  1. LDL receptor or ApoB-100
  2. LDL
  3. Premature coronary artery disease
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3
Q

Famililal Dysbetalipoproteinemia Syndrome

(Type 3 Familial Dyslipidemia)

  1. What protein is defected?
  2. What lipoprotein is elevated?
  3. What are the major clinical features?
A
  1. ApoE
  2. Chylomicrons and VLDL
  3. Premature coronary artery disease
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4
Q

Famililal hypertriglyceridemia Syndrome

(Type 4 Familial Dyslipidemia)

  1. What protein is defected?
  2. What lipoprotein is elevated?
  3. What are the major clinical features?
A
  1. ApoA-V
  2. VLDL
  3. increased pancretisis risk (associated with obesity and insulin resistance)
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5
Q

SIADH

  1. Plasma Sodium (High or Low)
  2. Plasma Osmolality (High or Low)
  3. Urine Osmolality (High or Low)
  4. Volume Status (High/Normal/Low)
A
  1. Low (due to retention of free-water)
  2. Low
  3. High
  4. Normal/Euvolemic
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6
Q

Primary Hyperaldosteronism

  1. What are the main causes?
  2. Aldosterone (high or low)
  3. Plasma Renin (high or low)
  4. Sodium Levels (high or Low)
  5. Edema (yes or no)
  6. Potassium Levels (high or Low)
A
  1. Bilateral Adrenal Hyperplasia or Adrenal Adenoma
  2. High
  3. Low
  4. NORMAL Na+ (due to aldosterone escape due to increased renal blood flow)
  5. No edema (due to aldosterone escape)
  6. Low
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7
Q

Secondary Hyperaldosteronism

  1. What are the main causes?
  2. Aldosterone (high or low)
  3. Plasma Renin (high or low)
  4. Sodium Levels (high or Low)
  5. Edema (yes or no)
  6. Potassium Levels (high or Low)
A
  1. Activation of Renin-Angiotensin System
  2. High
  3. High
  4. High
  5. Yes
  6. Low
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8
Q

Glucagonoma

  1. How is diagnosed?
  2. Clinical Presentation
A
  1. Elevated Glucagon levels
  2. Clinical presentation
  • Necrolytic migratory erythema (blistering eythemetous plaques with central clearing)
  • Hyperglycemia (often as a newly diagnosed diabetes)
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9
Q

Subacute Granulomatous Thyroiditis

  1. Etiology
  2. Clinical Symptoms
  3. Diagnostic Test
  4. Histology
A
  1. Following a viral ilness
  2. Clinical features:
  • Painful thyroid enlargement
  • Tender thyroid
  • Hyperthyroid symptoms
  1. Increased ESR (erythrocyte sedementation rate)
  2. Inflammatory infiltrate, macrophages and giant cells
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10
Q

Hashimoto Thyroiditis

  1. Etiology
  2. Clinical Symptoms
  3. Diagnostic Test
  4. Histology
A
  1. Autoimmune (HLA-DR3)
  2. Clinal features:
  • Painless thyroid enlargement
  • Nontender thyroid
  • Hypothyroid features (may be hyperthyroid at first)
  1. Positive TPO antibody
  2. Lymphocytic infiltate with germinal centers, Hurthle Cells
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11
Q

Pituitary Apoplexy

  1. What is it?
  2. When does it most commonly occur?
  3. How does it present?
  4. Complications
  5. Treatment
A
  1. Pituitary Hemorrage
  2. After a pituitary adenoma (therefore presents with a history of a pituitary adenoma symptoms)

3. Clinical features

  • Severe headache
  • Bitemporal hemianopsia (loss of temporal vision)
  • Opthalmoplegia (paralysis of surrounding eye muscles)
  • Altered conciousness

4. Complications

  • hypopituitarism
  • severe hypotension
  • coma & death

5. Glucocorticoids

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12
Q

Sheehan Syndrome

  1. What is it?
  2. When does it present?
  3. How does it present?
A
  1. Ischemic necrosis of the pituitary
  2. Most commonly after childbirth
  3. Clinical features
  • failure to lactate
  • absent menstruation
  • cold intolerance
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13
Q

What are the main causes of Hypopituitarism?

A
  1. Mass lesions (primary/metastatic)
  2. Infiltration & infection
  3. Hemorrage (pituitary apoplexy)
  4. Ischemic infarction (sheehan syndrome)
  5. Sarcoidosis
  6. Radiation therapy
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14
Q

What is an elevated serum creatine kinase indicative of?

What can cause this? (3)

A

Myopathy (muscle disease)

(1) Inflammatory Myopathies

  • muscle weakness
  • skin rash
  • inflammatory arthritis

(2) Statin-induced Myopathy

  • occurs weeks to months after starting statin therapy
  • muscle pain and weakness

(3) Hypothyroid Myopathy

  • delayed tendon reflexes
  • muscle pain, cramps, weakness
  • features of hypothyroidism
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15
Q

In which type of diabetes is the following seen?

(1) Pancreatic Islet infiltration with leukocytes
(2) Amyloid deposition
(3) Ketoacidosis

A

(1) Type I
(2) Type II
(3) Type I

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16
Q

The Metyrapone Stimulation Test

(1) What does it test?
(2) How?

A
  1. Tests Hypothalmic-Pituitary (HPA) Axis Integrity
  2. It blocks cortisol synthesis by inhibiting 11-ß-hydroxylase which with then lead to a rise of ACTH (to try and raise cortisol levels)
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17
Q

How will High-Dose Dexamethasone alter ACTH levels in the following causes of Cushing syndrome?

(1) Exogenous Glucocorticoids
(2) ACTH-secreting Pituitary Adenoma
(3) Ectopic ACTH secretion
(4) Adrenal Adenoma, Hyperplasia or Carcinoma

A

(1) No change (remains elevated)
(2) Decreased
(3) No change (remains elevated)
(4) No change (remains elevated)

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18
Q

How will Low-Dose Dexamethasone alter ACTH levels in the following causes of Cushing syndrome?

(1) Exogenous Glucocorticoids

(2) ACTH-secreting Pituitary Adenoma

(3) Ectopic ACTH secretion

(4) Adrenal Adenoma, Hyperplasia or Carcinoma

A

(1) No change (remains elevated)
(2) No change (remains elevated)
(3) No change (remains elevated)
(4) No change (remains elevated)

Low-Dose Dexamethasone will only supress ACTH in normal individuals

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19
Q

How will the following causes of Cushing Syndrome present?

(1) Exogenous Glucocorticoids

(2) ACTH-secreting Pituitary Adenoma

(3) Ectopic ACTH secretion

(4) Adrenal Adenoma, Hyperplasia or Carcinoma

A

(1) Bilateral adrenal atrophy

(2) Bilateral adrenal enlargement

(3) Small cell carcinoma or Carcinoid tumor

(4) 2 scenarios:

i. atrophy of the non-affected adrenal gland
ii. bilateral nodular hyperplasia (both affected)

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20
Q

(1) How to we assess long-term glycemic control in patients with diabetes?
(2) What can alter this assessment?

A

(1) We measure the HbA1c (glycated hemoglobin) levels.

(2)

  • Poor glycemic control will elevate HbA1c levels (Higher glucose levels and longer exposure of RBCs to to glucose will increase HbA1c levels)
  • Beta-thalassemia can falsely lower the HbA1c due to the decreased lifespan of the RBCs (there will also be an elevated HbA2)
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21
Q

Exogenous Hyperthyrodism

  1. What are the most common causes?
  2. Lab findings (T4, TSH, TG)
  3. Long-term Complications
A
  1. Levothyroxine abuse (to lose weight), Thyroid supplements, Improper dosing of thyroid replacement therapy
  2. Lab findings
  • increased T4
  • decreased TSH
  • low/undetectable thyroglobullin (TG)
    • normally a small amount is released
    • low levels are indicative of thyroid supression
  1. Thyroid follicles become atrophic with decreased colloid (due to lack of of TSH)
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22
Q

What are the effects of alcohol on glucose regulation and why?

Major complication?

A

Alcohol inhibits gluconeogenesis.

Ethanol inhibits the conversion of lactate to pyruvate which is an essential step of gluconeogenesis.

major complication:

Alcohol can cause hypoglycemia when hepatic glycogen stores are depeleted (since there will be no other way to make glucose)

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23
Q

How is MEN 1 charachterized? (3)

A
  1. Primary Hyperparathyroidism (parathyroid adenoma or hyperplasia)
  2. Pituitary Tumors (prolactinoma, visual distrubances, etc.)
  3. Pancreatic Tumors (especially gastrinomas)
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24
Q

How is MEN 2A charachterized? (3)

A
  1. Medullary Thyroid Cancer (secretes calcitonin)
  2. Pheochromocytoma (secretes catelcholamines)
  3. Primary Hyperparathyroidism (parathyroid adenoma or hyperplasia)
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25
Q

How is MEN 2B charachterized? (4)

A
  1. Medullary Thyroid Cancer (secretes calcitonin)
  2. Pheochromocytoma (secretes catelcholamines)
  3. Mucosal Neuromas (papules on lips, tongues, etc)
  4. Marfanoid habitus (long arms, long fingers)
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26
Q

MEN2 (both A & B) are associated with germinline mutations is what?

A

The RET proto-oncogene

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27
Q

Maternal Hyperglycemia

  1. Is it dangerous to the infant? Why?
  2. What can it cause in the infant?
A
  1. Yes

It causes increased transplacental glucose delivery to the baby –> fetal hyperglycemia-->beta cell hyperplasia–> fetal insulinemia

2.

  • Fetal Macrosomia (baby >4kg)
  • Hypoglycemia after delivery (due to the continued increased insulin but discontinued glucose from mother)
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28
Q

How does Type 1 diabetes typically present?

A
  • Polyuria
  • Polydipsia
  • Polyphagia
  • Weight Loss
  • Blurred vision
  • Ketoacidosis
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29
Q

How to we diagnose Type 1 diabetes? (4 ways)

A
  1. Fasting Glucose >126 mg/dL
  2. Random Glucose >200 mg/dL
  3. HbA1c > 6.5%
  4. Oral Glucose Tolerance Test
30
Q

How does Hypothyroidism typically present?

A
  1. Fatigue
  2. Weight Gain
  3. Constipation
  4. Bradycardia
  5. Hypertension
  6. Relaxation of deep tendon reflexes
  7. Alterations in Hair growth (thinning of scalp and eyebrows)
31
Q

Acromegaly

  1. What causes it?
  2. How does it present?
A
  1. Pituitary Somatotroph Adenoma

2.

  • Enlarged hands, jaw and feet
  • Eyebrow Protrusion
  • LV hypertrophy –> Heart Failure
  • Osteoarthritis
32
Q

What are the common endocrine paraneoplastic syndromes associated with lung cancer?

A
  1. SIADH (cant pee)
  2. Secretion of PTHrP (hypercalemia)

3. Paraneoplastic Cushing Syndrome

  • hypertension, hyperglycemia, edema and hyperpigmentation (inc. MSH)
33
Q

What are the effects of sex steroids (estrogen,testosterone) on growth?

A

Sex steroids both promote and inhibit growth.

They initially promote linear growth but then they inhibit it via closure of the epiphyseal growth plates.

34
Q

What is the growth pattern of someone who has undergone precocious puberty?

A

They will be very tall for their age at first due to an early growth spurt however they will likely be considered short when older.

This is due to sex hormones promoting growth early but also inhibiting growth early.

35
Q

Glucagon

  1. What does it activate?
  2. How does it work? (chemical pathway)
A
  1. It is used to elevate serum glucose levels by stimulating hepatic glycogenolysis and gluconeogenesis. It also stimulates insulin secretion from pancreas.

2.

  1. Stimulates G-protein coupled receptors
  2. increased cAMP
  3. Activation of PKA
  4. Activation of Glycogen phosphorylase
36
Q

Hashimoto Thyroiditis

  1. What is it?
  2. What is it associated with?
  3. How does it present?
  4. Labs (T4 and TSH levels)
  5. Histology
A
  1. Autoimmune destruction of thyroid

(Anithyroglobullin and Antithyroid-peroxidase ABs)

  1. HLA-DR5
  2. Hyperthyroidism initally and then Hypothyroidism
  3. Low T4 and High TSH
  4. Lymphocyte and plasma cells with germinal centers, Hurthle cells
37
Q

Reidel Thyroiditis

  1. How does it present?
  2. What are common complications?
  3. What is it often confused with?
A
  1. Hypothyroidism with a fibrosed hard non-tender thyroid
  2. Fibrosis can extend to airway (breathing issues) and esophagus (swallowing issues)

3. Anaplastic Carcinoma

  • both have hard thyroid
  • Carcinoma presents in older individuals (40+)
  • Carcinoma has malignant cells
38
Q
  1. What are the effects of Glucocorticoids/Steroids on the HPA axis?
  2. Can this lead to a major complication?
A

(1)

They inhibit the HPA axis

(most common cause of adrenal insufficiency)

  1. Steroids inhibit CRH from hypothalamus
  2. Decreased ACTH
  3. Decreased Cortisol

(2) Yes, in high stress situations (infections,surgery), cortisol will not be able to increase and this can lead to hypotension/shock

39
Q

Pheochromocytoma

  1. What is it?
  2. How does it present?
  3. How is diagnosed?
  4. What is seen on microscopy and immunohistochemistry?
A
  1. Tumor of chromaffin cells of adrenal medulla (secrete catelcholamines)
  2. Due to episodic release of catelcholamines, episodic symptoms sympathetic system
  3. Elevated urinary catelcholamines and metanephrines

4.

  • Electron-dense membrane bound secretary granules
  • + synaptophysin, chromogranin and enolase cells
40
Q

How does a prolactinoma present in?

A
  • Galactorrhea (increased prolactin)
  • Ammenorrhea (inhibition of GnRH)
  • Decreased Libido
  • Mass Effect (bitemopral hemianopsia, headaches)
41
Q

Klinefelter Syndrome

  1. What is it?
  2. Labs (LH, FSH, Test., Inhibin)
  3. How does it present?
A
  1. Hypogonadism due to destruction of seminiferous tubules and abnormal Leydig cells
  2. Labs:
  • Low inhibin levels (due to damaged sertoli cells)
  • Low testosterone levels (due to damaged leydig cells)
  • Increased LH & FSH (due to loss of negative feedback)
  1. Clinical Presentation
  • small, firm testes
  • gynecomastia (due to increased estrogen due to inc. LH)
  • no/low sperm count
42
Q

What is the consequence of having a disruption of the pituitary stalk?

A

This can disrupt the dopaminergic pathway of the stalk, which can cause loss of inhibition of prolactin.

43
Q

How Diabetic Ketoacidosis (DKA) affect potassium levels in the body?

A

Normal/Increased extracellular potassium

Decreased Intracellular Potassium

(98% of K is stored intracellularly so we have a total body deficit)

44
Q

21-Hydroxylase Deficiency

  1. Hormone Effects
  2. BP
  3. Sexual Characteristics
A

1.

  • Increased Sex hormones
  • Decreased Aldosterone & Cortisol
  1. Decreased BP (increased [K+])

3.

  • Males: appear normal
  • Females: virilization (develop male characteristics)
45
Q

17alpha-Hydroxylase Deficiency

  1. Hormones
  2. BP
  3. Sexual Characteristics
A

1.

  • Increased Aldosterone
  • Decreased Cortisol and Sex hormones

2. Increased BP

3.

  • Males: appear female at birth, appear male at puberty
  • Females: normal at birth, lack seocndary sexual development
46
Q

11alpha-Hydroxylase Deficiency

  1. Hormones
  2. BP
  3. Sexual Characteristics
A

1.

  • Increased Sex hormones & 11-deoxycorticosterone
  • decreased aldosterone and cortisol

2. Increased BP

3.

  • Males: appear normal
  • Females: virilization (have male characteristics)
47
Q

5alpha-reductase deficiency

  1. What does it prevent?
  2. How does it present?
A
  1. Inability to convert testosterone into DHT
  2. In males:
  • Male internal genitalia
  • Ambiguous external genitalia (until puberty)
48
Q

What are the effects of androgen abuse on following systems?

  1. Blood
  2. Skin
  3. Genitals
  4. Breast
A
  1. Increased Hematocrit & LDL
  2. Acne
  3. Testicular atrophy
  4. Gynecomastia
49
Q

What is the most common cause of death in patients with diabetes? Why?

A

Myocardial Infarction

Due to Nonenzymatic glycosylation of large vessels

50
Q

How do thiazide diuretics alter the levels of:

  1. Calcium
  2. PTH
A
  1. increased calcium
  2. decreased PTH

(due to increased calcium)

51
Q

What are the 3 endocrine paraneoplastic syndromes associated with lung cancer?

A
  1. Cushing syndrome: Ectopic ACTH production
  2. Hypercalcemia: secretion of PTHrp
  3. SIADH
52
Q

What mediates the growth-promoting effects of Growth Hormone?

A

IGF-1 released by the liver

53
Q

How would levels of the following be altered in a patient with celiac disease:

  1. Calcium
  2. Phosphorus
  3. PTH
A

(this patient will have Vitamin D, A, E, K deficiency due to celiac)

  1. decreased calcium
  2. decreased phosphorus

(Vitamin D increases absorption of Ca and P in SI)

  1. Increased PTH

(to try and raise Ca levels)

54
Q

Polycystic Ovary Syndrome (PCOS)

  1. How does it present?
  2. Treatment
A

1.

Hirsutism + Acne (Androgen Excess)

Mensrual irregularities (Ovarian dysfunction)

Insulin resistance

  1. Contraceptives (to decrease androgens)
55
Q

Why can oral contraceptives be used to treat Hirsutism?

A

They suppress LH secretion which decreases ovarian androgen production

56
Q

In a patient with adrenal insufficiency would the following be increased or decreased:

  1. Sodium
  2. Potassium
  3. H+
  4. Bicarbonate (HCO3)
A
  1. decreased sodium
  2. increased potassium
  3. increased H+
  4. decreased bicarbonate
57
Q

In a patient with osteoporosis due to primary hyperparathyroidism, what part of the bone is most likely to be affected?

How does it appear?

A

Cortical part of the bone

Cortical thinning

58
Q

How can TNF-alpha cause insulin resistance?

A

It activates serine kinases which inhibits tyrosine phosphorylation

59
Q

Gynecomastia

  1. Pathophysiology
  2. How/why does this occur?
A

1. Increased estrogen/androgen ratio

2.

increased estrogen–> cirrhosis, obesity

decreased testosterone –> CKD, hypogonadism

Medications: Ketoconazole, 5-alpha reductase inhibitors, spironolactone

60
Q

What is the primary regulator of the:

  1. Zona Glomerulosa
  2. Zona Fasciculata
  3. Zona Reticularis
A
  1. Angiotensin II —> aldosterone
  2. ACTH —> cortisol
  3. ACTH —> androgens
61
Q

Why can alcohol cause hypoglycemia?

A

Inhibits gluconeogenesis

(due to increased NADH/NAD+ ratio)

62
Q

Primary Adrenal Insufficiency

  1. How does it present?
  2. How is it treated?
A

1.

Hypotension, nausea/vomitting, abdominal pain, hyperpigmentation

2.

Hydrocortisone or Dexamethasone + Glucocorticoids + Fluids

63
Q

A 3 week postpartum women has still not lactated and has absent menstruation.

What is the most likely diagnosis?

Why does this occur?

A

Sheehan Syndrome

Ischemic infact of the pituitary following pregancy

Occurs due to the pituitary enlarging during pregnancy while the blood supply does not increase proportionally

64
Q

Why does excessive weight loss, strenous exercise and eating disorders cause ammenorhea?

A

Decreased adipose tissue —> decreased leptin

—–> decreased GnRH from hypothalamus

—–> decreased LH & FSH from pituitary

——> decreased estrogen production in ovaries

——> amenorrhea + bone loss

65
Q

How does chronic exogenous steroid/glucocorticoid therapy affect the hypothalamus-pituitary-adrenal (HPA) axis?

A

It impairs the HPA axis (tertiary adrenal insufficiency)

  • decreased CRH from hypothalamus
  • decreased ACTH from pituitary
  • decreased cortisol from adrenals
66
Q

Gynecomastia

  1. What is it?
  2. What is its pathophysiology?
A
  1. Development of glandular breast tissue in males

2.

Increased estrogen to androgen ratio

67
Q

What should be given to a patient with adrenal insufficiency undergoing an adrenal crisis?

A

Glucocorticoids (hydrocortisone or dexamethasone)

Since they cannot increase glucocorticoid production during an acute stress

68
Q

Kallmann Syndrome

  1. How does it present
  2. Why/How does it occur?
A

1.

Hypogonadism, delayed puberty, lack of smell

2.

Abscense of GnRH secretory neurons in the hypothalamus

69
Q

In a patien with primary hyperparathyroidism, what potential associated conditions may be found in this patient?

A

Nephrolithiasis (Calcium kidney stones)

Constipation

70
Q

Adrenal Insufficiency

  1. How does it present?
  2. Lab findings
    - Sodium
    - Potassium
    - H+
    - Bicarbonate
A
  1. Fatigue, weakness, weight loss, hypotension, hyperpigmentation (due to inc. ACTH)
    • Low sodium

- High Potassium

- High H+

- Low Bicarbonate

71
Q

How would a Prolactinoma affect the following:

  1. GnRH
  2. LH
  3. Testosterone
A

Decreased GnRH

Decreased LH

Decreased Testosterone

UWorld - Endocrine (2 decks)

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