Sweep 1.3 Flashcards
o zona glomerulosa –
mineralcorticoids (aldosterone)
o zone fasciculata –
glucocorticoids (cortisol)
o zona reticularis –
sex hormones (estrogen/androgen)
Hypercortisolism (Cushing Syndrome)
• Causes
o Most commonly by excess administration of —————
o ————– (e.g. adrenal adenoma)
exogenous glucocorticoids
Primary adrenal hyperplasia or neoplasm
Hypercortisolism (Cushing Syndrome)
Causes
o Primary pituitary source
• ACTH oversecretion by ————-
pituitary microadenoma
Hypercortisolism (Cushing Syndrome)
Causes
o Ectopic ——– secretion by ——-, e.g. lung
ACTH
neoplasm
Hypercortisolism (Cushing Syndrome)
• Signs and symptoms
o Short Term
- weight gain and hypertension
- “Moon facies” (accumulation of fat in the face)
- “Buffalo hump” (accumulation of fat in the posterior neck and back)
Hypercortisolism (Cushing Syndrome)
• “Moon facies”
(accumulation of fat in the face)
Hypercortisolism (cushing syndrome)
• “Buffalo hump”
(accumulation of fat in the posterior neck and back)
Hypercortisolism (cushing syndrome)
• Signs and symptoms
o Long Term
- Decreased muscle mass, weakness
- Diabetes
- Osteoporosis
- Cutaneous striae, hirsutism
- Mental disturbances: mood swings, depression, psychosis
- Menstrual irregularities
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: —————-
acute stress
• Vomiting, abdominal pain, hypotension, coma, death
IV. Adrenal Neoplasms
• Pheochromocytoma
o neoplasm of ———, F > M, 30-60 yrs. ——— cells produce
————.
chromaffin cells
Chromaffin
epinephrine
IV. Adrenal Neoplasms
• Pheochromocytoma
Symptoms
o Hypertension, tachycardia, tremor, headache
IV. Adrenal Neoplasms
• Pheochromocytoma
o Surgically ———-
correctible
IV. Adrenal Neoplasms
• Pheochromocytoma
o rule of 10’s: 10 % ————–
bilateral, extra-adrenal, malignant, familial syndromes
IV. Adrenal Neoplasms
• Pheochromocytoma
o large ———– with variable ————
polygonal cells
pleomorphism
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
Most common
Lobulated
encapsulated
Epithelial and myoepithelial
B. Salivary gland tumors
Benign
b. Warthin tumor (papillary cystadenoma lymphomatosum)
1. Primarily affects ———-
2. ———– with papillary ———– and lymphoid tissue
3. 10% ———
parotid gland
Cystic neoplasm
infoldings
bilateral
B. Salivary gland tumors
2. Malignant a. Mucoepidermoid carcinoma:
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
II. Esophagus
A. Obstruction
1. Mechanical:
Post-inflammatory fibrosis/stenosis
II. Esophagus
Obstruction
2. Functional:
Discoordinated muscular contractions or spasms, diverticula may result;
achalasia (inability of lower esophageal sphincter to relax) difficulty in swallowing
II. Esophagus
achalasia
(inability of lower esophageal sphincter to relax) difficulty in swallowing
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
portal hypertension
cirrhotic
asymptomatic
II. Esophagus
D. Barrett Esophagus
1. ———— within the esophagus squamous mucosa
Intestinal metaplasia
II. Esophagus
Barrett Esophagus
3. Diagnostic features for Barrett esophagus:
1) extension abnormal mucosa above ————
2) demonstration of ————- (intestinal metaplasia).
gastro-esophageal junction,
squamous metaplasia
A. Pancreatic anatomy
a. Acute Pancreatitis
• Reversible ——– injury associated with inflammation,
parenchymal
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.
biliary tract disease
alcoholism
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 ———-
ABDOMINAL PAIN
toxic enzymes..
a. Cholangiocarcinoma (CCA)
• Cancer of ——–most are adenoCAs
• Very ———– tumor-tumors are ———-
biliary tree
desmoplastic
firm and gritty
Cholangiocarcinoma
• Can get ——— with HCC
• ——– until late stage
• Generally fatal within ———
collision tumor
Asymptomatic
6 months
Hepatoblastoma • Most common liver tumor in ----------- • --------- type • Mixed ----------- • Treatment------------ then ---------- • Is rapidly fatal (within months) if not treated
young pediatric patients
Epithelioid
epithelial-mesenchymal
chemotherapy
surgical resection
c. Hepatocellular adenoma
• Benign
• Association with ————, if discontinued, may regress
oral contraceptives
Hepatocellular adenoma
• Presentation
- Acute abdomen
- Intra-abdominal bleed
- Histology: bland hepatocytes and no bile ducts
d. Hepatocellular Carcinoma
• Fibrolamellar variant
o Young males and females (20-40 yo)
o Distinct from HCC
o No known risk factors
o “Scirrhous tumor”
Hepatocellular carcinoma
o Patients generally do NOT have
underlying liver disease-better prognosis.
Hepatocellular carcinoma
o Treatment:
Surgery
o Better prognosis (32 % 5 yr survival)
I. Liver Nodules and Tumors
- Nodular hyperplasia- ———– may develop
single or multiple nodules
I. Liver Nodules and Tumors
Nodular hyperplasia
a. In a non-cirrhotic liver
“focal nodular hyperplasia” or “nodular regenerative hyperplasia”
I. Liver Nodules and Tumors
Nodular hyperplasia
b. Common factor-
focal or diffuse alteration in hepatic blood supply, resulting in obliteration of the portal veins and a compensatory increase in arterial supply
Benign liver neoplasms.
b. Cavernous ————–
c. ———–increase in young women using oral contraceptives
hemangioma
Hepatic adenoma
Benign Liver Neoplasms
d. Concerns with these:
1) mimic HCC, 2) subcapsular hemorrhage-from a rupture and bleed, 3) may transform to HCC.
Benign liver neoplasms
e. Are associated with ———-
hormonal stimulation
A. Stomach-reactive lesions
Acute and chronic gastritis
- Acute gastritis
• Abrupt, transient
• Pathogenesis:
Cigarettes, Alcohol, Stress, Ischemia, NSAID’s, aspirin, infection
- Acute gastritis
• May range from ———– May develop ———-.
asymptomatic to pain, nausea and vomiting.
erosion and/or hemorrhage
- Acute gastritis
• Pathology:
Punctate hemorrhage, erosion, edema, acute inflammation
- Chronic gastritis
• Primarily caused by infection with ———
• Often acquire the infection in ———.
Helicobacter pylori in patients with H. pylori (spiral or curved bacilli): 90% of cases.
childhood
- Chronic gastritis
• Treatment with ——— and ———- inhibitors.
antibiotics
proton pump
- Chronic gastritis
• ————: 10 % of cases (E.g. Pernicious Anemia
• Pathology: —————–
Autoimmune-gastritis
Atrophic epithelium, chronic inflammation, intestinal metaplasia
- Chronic gastritis
• Clinical course:
Ulceration, cancer risk 2-4% (intestinal metaplasia)
