Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

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

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
How is **_MEN 2B_** charachterized? (4)
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)
26
MEN2 (both A & B) are associated with germinline mutations is what?
The RET proto-oncogene
27
**_Maternal Hyperglycemia_** 1. Is it dangerous to the infant? Why? 2. What can it cause in the infant?
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)
28
How does Type 1 diabetes typically present?
* Polyuria * Polydipsia * Polyphagia * Weight Loss * Blurred vision * Ketoacidosis
29
How to we diagnose Type 1 diabetes? (4 ways)
1. **Fasting Glucose \>126** mg/dL 2. **Random Glucose \>200** mg/dL 3. **HbA1c \> 6.5%** 4. **Oral Glucose Tolerance Test**
30
How does **Hypothyroidism** typically present?
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
**_Acromegaly_** 1. What causes it? 2. How does it present?
1. Pituitary **Somatotroph** Adenoma 2. * Enlarged hands, jaw and feet * Eyebrow Protrusion * **LV hypertrophy** --\> Heart Failure * **Osteoarthritis**
32
What are the common **endocrine paraneoplastic syndromes** associated with **lung cancer**?
1. **_SIADH_** (cant pee) 2. **_Secretion of PTHrP_** (hypercalemia) **_3. Paraneoplastic Cushing Syndrome_** * hypertension, hyperglycemia, edema and **hyperpigmentation** (inc. MSH)
33
What are the effects of **sex steroids** (estrogen,testosterone) on **growth**?
Sex steroids both promote and inhibit growth. They i**nitially promote linear growth** but then they **inhibit it via closure of the epiphyseal growth plates.**
34
What is the growth pattern of someone who has undergone **precocious puberty**?
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
**_Glucagon_** 1. What does it activate? 2. How does it work? (chemical pathway)
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
**_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
1. Autoimmune destruction of thyroid (**Anithyroglobullin** and **Antithyroid-peroxidase** ABs) 2. **HLA-DR5** 3. **Hyperthyroidism** initally and then **_Hypothyroidism_** 4. Low T4 and High TSH 5. Lymphocyte and plasma cells with **germinal centers**, **Hurthle cells**
37
**_Reidel Thyroiditis_** 1. How does it present? 2. What are common complications? 3. What is it often confused with?
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
1. What are the effects of **Glucocorticoids/Steroids** on the **HPA axis?** 2. Can this lead to a major complication?
(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
**_Pheochromocytoma_** 1. What is it? 2. How does it present? 3. How is diagnosed? 4. What is seen on microscopy and immunohistochemistry?
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
How does a **prolactinoma** present in?
* **Galactorrhea** (increased prolactin) * **Ammenorrhea** (inhibition of GnRH) * **Decreased Libido** * **Mass Effect** (bitemopral hemianopsia, headaches)
41
**_Klinefelter Syndrome_** 1. What is it? 2. Labs (LH, FSH, Test., Inhibin) 2. How does it present?
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) 3. Clinical Presentation * **small, firm testes** * **gynecomastia** (due to increased estrogen due to inc. LH) * **no/low sperm count**
42
What is the consequence of having a **disruption of the pituitary stalk**?
This can **disrupt the dopaminergic pathway of the stalk**, which can cause loss of inhibition of prolactin.
43
How **Diabetic Ketoacidosis** (DKA) affect **potassium** levels in the body?
**Normal/Increased _extracellular_ potassium** **Decreased _Intracellular_ Potassium** (98% of K is stored intracellularly so we have a **total body deficit**)
44
**_21-Hydroxylase Deficiency_** 1. Hormone Effects 2. BP 3. Sexual Characteristics
1. * **Increased Sex hormones** * Decreased Aldosterone & Cortisol 2. **Decreased BP** (increased [K+]) 3. * **Males:** appear normal * **Females**: virilization (develop male characteristics)
45
**_17alpha-Hydroxylase Deficiency_** 1. Hormones 2. BP 3. Sexual Characteristics
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
**_11alpha-Hydroxylase Deficiency_** 1. Hormones 2. BP 3. Sexual Characteristics
1. * **Increased Sex hormones & 11-deoxycorticosterone** * decreased aldosterone and cortisol **2. Increased BP** 3. * **Males**: appear normal * **Females**: virilization (have male characteristics)
47
**_5alpha-reductase deficiency_** 1. What does it prevent? 2. How does it present?
1. Inability to convert **testosterone** into **DHT** 2. _In males_: * **Male internal genitalia** * **Ambiguous external genitalia** (until puberty)
48
What are the effects of **androgen abuse** on following systems? 1. Blood 2. Skin 3. Genitals 4. Breast
1. Increased **Hematocrit** & **LDL** 2. Acne 3. Testicular atrophy 4. Gynecomastia
49
What is the most common cause of death in patients with diabetes? Why?
Myocardial Infarction Due to Nonenzymatic glycosylation of large vessels
50
How do thiazide diuretics alter the levels of: 1. Calcium 2. PTH
1. increased calcium 2. decreased PTH (due to increased calcium)
51
What are the 3 endocrine paraneoplastic syndromes associated with lung cancer?
1. **_Cushing syndrome_**: Ectopic ACTH production 2. **_Hypercalcemia_**: secretion of PTHrp 3. **_SIADH_**
52
What mediates the growth-promoting effects of **Growth Hormone?**
**_IGF-1_** released by the **_liver_**
53
How would levels of the following be altered in a patient with celiac disease: 1. Calcium 2. Phosphorus 3. PTH
(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) 3. **Increased PTH** (to try and raise Ca levels)
54
Polycystic Ovary Syndrome (PCOS) 1. How does it present? 2. Treatment
1. Hirsutism + Acne (Androgen Excess) Mensrual irregularities (Ovarian dysfunction) Insulin resistance 2. Contraceptives (to decrease androgens)
55
Why can oral contraceptives be used to treat **_Hirsutism_**?
They **suppress LH secretion** which **decreases ovarian androgen production**
56
In a patient with **adrenal insufficiency** would the following be increased or decreased: 1. Sodium 2. Potassium 3. H+ 4. Bicarbonate (HCO3)
1. decreased sodium 2. increased potassium 3. increased H+ 4. decreased bicarbonate
57
In a patient with **osteoporosis** due to **primary hyperparathyroidism**, what part of the bone is most likely to be affected? How does it appear?
**Cortical** part of the bone **Cortical thinning**
58
How can **TNF-alpha** cause insulin resistance?
It **_activates serine kinases_** which inhibits tyrosine phosphorylation
59
**_Gynecomastia_** 1. Pathophysiology 2. How/why does this occur?
**1. Increased estrogen/androgen ratio** 2. increased estrogen--\> **cirrhosis, obesity** decreased testosterone --\> **CKD, hypogonadism** Medications: **Ketoconazole, 5-alpha reductase inhibitors, spironolactone**
60
What is the primary regulator of the: 1. Zona Glomerulosa 2. Zona Fasciculata 3. Zona Reticularis
1. **Angiotensin II** ---\> aldosterone 2. **ACTH** ---\> cortisol 3. **ACTH** ---\> androgens
61
Why can alcohol cause hypoglycemia?
**Inhibits gluconeogenesis** | (due to increased NADH/NAD+ ratio)
62
**_Primary Adrenal Insufficiency_** 1. How does it present? 2. How is it treated?
1. **Hypotension**, nausea/vomitting, **abdominal pain**, **hyperpigmentation** 2. **Hydrocortisone or Dexamethasone** + **Glucocorticoids** + **Fluids**
63
A 3 week postpartum women has still not lactated and has absent menstruation. What is the most likely diagnosis? Why does this occur?
**_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
Why does excessive weight loss, strenous exercise and eating disorders cause **ammenorhea**?
Decreased **adipose tissue** ---\> decreased **leptin** -----\> **decreased GnRH from hypothalamus** -----\> decreased **LH & FSH** from pituitary ------\> decreased **estrogen** production in ovaries ------\> amenorrhea + bone loss
65
How does **chronic exogenous steroid/glucocorticoid** therapy affect the **hypothalamus-pituitary-adrenal (HPA) axis**?
It impairs the HPA axis (tertiary adrenal insufficiency) - **decreased CRH** from hypothalamus - **decreased ACTH** from pituitary - **decreased cortiso**l from adrenals
66
**_Gynecomastia_** 1. What is it? 2. What is its pathophysiology?
1. Development of **glandular** breast tissue in males 2. Increased **estrogen to androgen ratio**
67
What should be given to a patient with **adrenal insufficiency** undergoing an **adrenal crisis?**
**_Glucocorticoids (hydrocortisone or dexamethasone)_** Since they cannot increase glucocorticoid production during an acute stress
68
**_Kallmann Syndrome_** 1. How does it present 2. Why/How does it occur?
1. Hypogonadism, delayed puberty, **lack of smell** 2. **Abscense of GnRH secretory neurons in the hypothalamus**
69
In a patien with primary hyperparathyroidism, what potential associated conditions may be found in this patient?
**_Nephrolithiasis_ (Calcium kidney stones)** Constipation
70
**_Adrenal Insufficiency_** 1. How does it present? 2. Lab findings - Sodium - Potassium - H+ - Bicarbonate
1. Fatigue, weakness, weight loss, hypotension, **hyperpigmentation (due to inc. ACTH)** 2. - **Low sodium** **- High Potassium** **- High H+** **- Low Bicarbonate**
71
How would a **_Prolactinoma_** affect the following: 1. GnRH 2. LH 3. Testosterone
**Decreased GnRH** **Decreased LH** **Decreased Testosterone**

UWorld - Endocrine (2 decks)

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