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Gen Path Final > Sweep 1.3 > Flashcards

Sweep 1.3 Flashcards

1
Q

o zona glomerulosa –

A

mineralcorticoids (aldosterone)

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2
Q

o zone fasciculata –

A

glucocorticoids (cortisol)

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3
Q

o zona reticularis –

A

sex hormones (estrogen/androgen)

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4
Q

Hypercortisolism (Cushing Syndrome)

• Causes
o Most commonly by excess administration of —————
o ————– (e.g. adrenal adenoma)

A

exogenous glucocorticoids

Primary adrenal hyperplasia or neoplasm

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5
Q

Hypercortisolism (Cushing Syndrome)
Causes
o Primary pituitary source
• ACTH oversecretion by ————-

A

pituitary microadenoma

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6
Q

Hypercortisolism (Cushing Syndrome)
Causes
o Ectopic ——– secretion by ——-, e.g. lung

A

ACTH

neoplasm

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7
Q

Hypercortisolism (Cushing Syndrome)
• Signs and symptoms
o Short Term

A
  • weight gain and hypertension
  • “Moon facies” (accumulation of fat in the face)
  • “Buffalo hump” (accumulation of fat in the posterior neck and back)
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8
Q

Hypercortisolism (Cushing Syndrome)

• “Moon facies”

A

(accumulation of fat in the face)

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9
Q

Hypercortisolism (cushing syndrome)

• “Buffalo hump”

A

(accumulation of fat in the posterior neck and back)

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10
Q

Hypercortisolism (cushing syndrome)
• Signs and symptoms
o Long Term

A
  • Decreased muscle mass, weakness
  • Diabetes
  • Osteoporosis
  • Cutaneous striae, hirsutism
  • Mental disturbances: mood swings, depression, psychosis
  • Menstrual irregularities
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11
Q

Acute Adrenocortical Insufficiency
• In patients maintained on exogenous corticosteroids, rapid withdrawal of steroids or failure to increase steroids in response to an ———- can precipitate an adrenal crisis

See: —————-

A

acute stress

• Vomiting, abdominal pain, hypotension, coma, death

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12
Q

IV. Adrenal Neoplasms
• Pheochromocytoma
o neoplasm of ———, F > M, 30-60 yrs. ——— cells produce
————.

A

chromaffin cells

Chromaffin

epinephrine

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13
Q

IV. Adrenal Neoplasms
• Pheochromocytoma
Symptoms

A

o Hypertension, tachycardia, tremor, headache

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14
Q

IV. Adrenal Neoplasms
• Pheochromocytoma
o Surgically ———-

A

correctible

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15
Q

IV. Adrenal Neoplasms
• Pheochromocytoma
o rule of 10’s: 10 % ————–

A

bilateral, extra-adrenal, malignant, familial syndromes

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16
Q

IV. Adrenal Neoplasms
• Pheochromocytoma
o large ———– with variable ————

A

polygonal cells

pleomorphism

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17
Q 
B.  	Salivary gland tumors
Benign
	 a.	Pleomorphic adenoma (mixed tumor)
		1.  ---------- neoplasm, 60% occur in parotid
		2.  -----------, firm on palpation
		3.  Variably ----------
		4.  -------------- components
		5.  10% recurrences
		6.  May undergo malignant transformation
A

Most common

Lobulated

encapsulated

Epithelial and myoepithelial

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18
Q

B. Salivary gland tumors
Benign
b. Warthin tumor (papillary cystadenoma lymphomatosum)
1. Primarily affects ———-
2. ———– with papillary ———– and lymphoid tissue
3. 10% ———

A

parotid gland

Cystic neoplasm

infoldings

bilateral

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19
Q

B. Salivary gland tumors

2. Malignant
 a. Mucoepidermoid carcinoma:
A

squamous and mucous cells

	1. Most common SG malignancy
	2. Parotid and minor glands
	3. May note bluish color due to mucin and cystic growth pattern
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20
Q

II. Esophagus

A. Obstruction
1. Mechanical:

A

Post-inflammatory fibrosis/stenosis

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21
Q

II. Esophagus
Obstruction
2. Functional:

A

Discoordinated muscular contractions or spasms, diverticula may result;
achalasia (inability of lower esophageal sphincter to relax) difficulty in swallowing

22
Q

II. Esophagus

achalasia

A

(inability of lower esophageal sphincter to relax) difficulty in swallowing

23
Q

II. Esophagus

B. Esophageal varices

1. Arise due to --------
2. Seen in 90% of --------- patients
3. Often --------, but rupture can result in massive hemorrhage/death
A

portal hypertension

cirrhotic

asymptomatic

24
Q

II. Esophagus

D. Barrett Esophagus
1. ———— within the esophagus squamous mucosa

A

Intestinal metaplasia

25
Q

II. Esophagus
Barrett Esophagus
3. Diagnostic features for Barrett esophagus:

1) extension abnormal mucosa above ————
2) demonstration of ————- (intestinal metaplasia).

A

gastro-esophageal junction,

squamous metaplasia

26
Q

A. Pancreatic anatomy
a. Acute Pancreatitis
• Reversible ——– injury associated with inflammation,

A

parenchymal

27
Q

Acute pancreatitis
• 80% of cases related to ———– or ——–; infections e.g. mumps, trauma, metabolic diseases (e.g. hypercalcemic states), medications (e.g. estrogens, chemotherapy), idiopathic.

A

biliary tract disease

alcoholism

28
Q

Acute pancreatitis
• Symptoms are ———-. This is the cardinal manifestation. “upper back intense pain”. Full blown acute pancreatitis is a medical emergency due to the potential to release ———-

A

ABDOMINAL PAIN

toxic enzymes..

29
Q

a. Cholangiocarcinoma (CCA)
• Cancer of ——–most are adenoCAs
• Very ———– tumor-tumors are ———-

A

biliary tree

desmoplastic

firm and gritty

30
Q

Cholangiocarcinoma
• Can get ——— with HCC
• ——– until late stage
• Generally fatal within ———

A

collision tumor

Asymptomatic

6 months

31
Q 
Hepatoblastoma
•	Most common liver tumor in -----------
•	--------- type
•	Mixed -----------
•	Treatment------------ then ----------
•	Is rapidly fatal (within months) if not treated
A

young pediatric patients

Epithelioid

epithelial-mesenchymal

chemotherapy

surgical resection

32
Q

c. Hepatocellular adenoma
• Benign
• Association with ————, if discontinued, may regress

A

oral contraceptives

33
Q

Hepatocellular adenoma

• Presentation

A
  • Acute abdomen
  • Intra-abdominal bleed
  • Histology: bland hepatocytes and no bile ducts
34
Q

d. Hepatocellular Carcinoma

• Fibrolamellar variant

A

o Young males and females (20-40 yo)
o Distinct from HCC
o No known risk factors
o “Scirrhous tumor”

35
Q

Hepatocellular carcinoma

o Patients generally do NOT have

A

underlying liver disease-better prognosis.

36
Q

Hepatocellular carcinoma

o Treatment:

A

Surgery

o Better prognosis (32 % 5 yr survival)

37
Q

I. Liver Nodules and Tumors

  1. Nodular hyperplasia- ———– may develop
A

single or multiple nodules

38
Q

I. Liver Nodules and Tumors
Nodular hyperplasia

a. In a non-cirrhotic liver

A

“focal nodular hyperplasia” or “nodular regenerative hyperplasia”

39
Q

I. Liver Nodules and Tumors
Nodular hyperplasia

b. Common factor-

A

focal or diffuse alteration in hepatic blood supply, resulting in obliteration of the portal veins and a compensatory increase in arterial supply

40
Q

Benign liver neoplasms.

b. Cavernous ————–
c. ———–increase in young women using oral contraceptives

A

hemangioma

Hepatic adenoma

41
Q

Benign Liver Neoplasms

d. Concerns with these:

A

1) mimic HCC, 2) subcapsular hemorrhage-from a rupture and bleed, 3) may transform to HCC.

42
Q

Benign liver neoplasms

e. Are associated with ———-

A

hormonal stimulation

43
Q

A. Stomach-reactive lesions

A

Acute and chronic gastritis

44
Q
  1. Acute gastritis
    • Abrupt, transient
    • Pathogenesis:
A

Cigarettes, Alcohol, Stress, Ischemia, NSAID’s, aspirin, infection

45
Q
  1. Acute gastritis

• May range from ———– May develop ———-.

A

asymptomatic to pain, nausea and vomiting.

erosion and/or hemorrhage

46
Q
  1. Acute gastritis

• Pathology:

A

Punctate hemorrhage, erosion, edema, acute inflammation

47
Q
  1. Chronic gastritis
    • Primarily caused by infection with ———
    • Often acquire the infection in ———.
A

Helicobacter pylori in patients with H. pylori (spiral or curved bacilli): 90% of cases.

childhood

48
Q
  1. Chronic gastritis

• Treatment with ——— and ———- inhibitors.

A

antibiotics

proton pump

49
Q
  1. Chronic gastritis
    • ————: 10 % of cases (E.g. Pernicious Anemia
    • Pathology: —————–
A

Autoimmune-gastritis

Atrophic epithelium, chronic inflammation, intestinal metaplasia

50
Q
  1. Chronic gastritis

• Clinical course:

A

Ulceration, cancer risk 2-4% (intestinal metaplasia)

Gen Path Final (18 decks)

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