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MD4001 Week 11 > 4. Pathology of the adrenal gland and endocrine pancreas.pdf > Flashcards

4. Pathology of the adrenal gland and endocrine pancreas.pdf Flashcards

1
Q

Examples of adrenal hyperfunction?

A
  • Cushing’ssyndrome
  • Conn’ssyndrome
  • Adrenogenital syndrome & congenital adrenal hyperplasia
  • Adrenocortical neoplasms
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2
Q

What is cushing’s syndrome?

A

Excessive secretion of cortisone

Also has mineralocorticoid effects

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3
Q

Clinical features of cushing’s syndrome?

A
  • Muscle catabolism
  • Fat: Moon fat,buffalo hump
  • Abnormal collagen maturation
  • Hypertension
  • Osteporosis
  • Impaired glucose tolerance
  • Hirsutism
  • Depression/psychosis
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4
Q

Causes of cushing’s syndrome?

A

Approx 2/3
• Pituitary adenoma producing ACTH > adrenal hyperplasia

Approx 1/6
• Primary adrenal neoplasm –
benign and malignant 50:50

Approx 1/6
• Ectopic ACTH or related
peptides > adrenal hyperplasia
• Iatrogenic > adrenal atrophy

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5
Q

What is the underlying cause of Conn’s syndrome?

A

Primary hyperaldosteronism

80% have adrenal adenoma
20% bilateral hyperplasia of zona glomerulosa but unknown cause

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6
Q

Signs of Conn’s

A 
• Hypokalaemia
• Muscle weakness and
cramps
• Metabolic alkalosis
• High aldosterone
• Low renin
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7
Q

Cause of secondary hyperaldosteronism?

A

Note: Secondary hyperaldosteronism Increased renin-angiotensin activity eg as a result of renal ischaemia

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8
Q

Why is steroid metabolism pathway important?

A

All products are made from same origin (cholesterol) so any change in pathways has many different steroidal impacts

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9
Q

Congenital adrenal hyperplasia, examples?

A

Uncommon but not impossible to see
1 in 15,000
• 21 hydroxylase deficiency (CYP21)
• 11-beta hydroxylase deficiency

Leads to abnormally functioning adrenals so loss of negative feedback system to pituitary –> Hyperplasia

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10
Q

Types of adrenal neoplasms?

A

Benign: Adrenal adenoma

Malignant:
Primary: @cortex and medulla 
Secondary: From...
-Lung
-Breast
-Kidney
-Colon
-Melanoma
-Lymphoma
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11
Q

Adrenal adenoma?

A
  • Notinfrequentat autopsy but only diagnosed in life if functional
  • Low malignant potential so treat conservatively

Normally non-functional

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12
Q

Prognosis of adrenal carcinoma

A

Radiotherapy/chemo/surgery ineffective

Poor outlook

Normally indicates advanced cancer

Rare

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13
Q

Sign of adrenal carcinoma?

A

Hirsutism
Why? As more often secrete sex steroids

Indicates fast growing neoplasm

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14
Q

Molecular changes in adrenal neoplasma?

A

Use?

  1. possible use in distinguishing adenoma from carcinoma – limited use
  2. identification of familial syndromes
Expression:
in carcinoma
• Proliferation markers up 
• Mutant p53 protein up 
• IGF II up
• EGFRup

Mutation:
• P53
• MEN1

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15
Q

Original and result of a phaechromocytoma?

A

Origin: Chromaffin cells

Results in… Intermittent production of catecholamines so episodic presentation

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16
Q

Presentation of phaechromocytoma?

A
  • Hypertension
  • Sweating
  • collapse
  • Glycosuria

Episodic symptoms. Induced by stress and physically squeezing the kidneys

17
Q

Phaechromocytoma…
• 20% ____, may be part of MEN
• Spectrum of benign to frankly malignant (____%)

A

Phaechromocytoma…
• 20% familial, may be part of MEN
• Spectrum of benign to frankly malignant (10%)

18
Q

Neuroblastoma, who?

What makes a worse prognosis?

A

Very rare, in young children

Worse in:

  • N-myc amplification
  • Adrenal site
19
Q

Examples of adrenal hypofunction acute and chronic conditions?

A

Acute:
-Meningococcal septicaemia
Leads to Disseminated intravascular coagulation (DIC) is a pathological process characterized by the widespread activation of the clotting cascade that results in the formation of blood clots in the small blood vessels throughout the body.

Chronic:

  • Addition’s disease (addison’s dsiease)
  • Amyloid
  • TB
  • Mets
20
Q

Signs of addison’s disease?

A
  • Lethargy • Weakness
  • Anorexia
  • Pigmentation of skin and mucous membranes
21
Q

Cause of Addison’s disease?

A
  • Autoimmuneadrenalitis >75%
  • Tuberculosis
  • Amyloid
  • Metastasis
22
Q

Associations of addison’s disease

A
  • Vitiligo

* Diabetes

23
Q

Epidemiology of DM1?

A 
• Under40, childhood
• Thin
• 1 in 500 
• 40%concordancein
mono-zygotic twins
24
Q

Epidemiology of DM2?

A
  • Over 40y
  • Obese
  • 1:50
25
Q

What is Hyperosmolar hyperglycemic state?

A

Hyperosmolar hyperglycemic state (HHS) is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis. Symptoms include signs of dehydration, weakness, legs cramps, trouble seeing, and an altered level of consciousness.

26
Q

T2DM:
MHCII linkage?
Autoantibodies to islets?
Amyloid?

A

MHCII linkage? No
Autoantibodies to islets? No, beta cells persist
Amyloid? Yes

27
Q

Name 3 other causes for diabetes?

A
  • Pancreatitis

* Cysticfibrosis • Tumour

28
Q

Consequence of ectopic cell tumour in the islets of langerhans?

A

VIPOMA
Ectopic hormone production of Vasoactive Intestinal Peptide –>
Verner-Morrision syndrome (pancreatic cholera)

This leads to:

  • Achlorhhydria
  • Diarrhoea
  • Hypokalaemia
  • Acidosis
  • Hypovolaemia

GASTRINOMA
Ectopic hormone production of gastrin, this is a G-cell tumour
–> Zollinger-ellison syndrome

Leads to:

  • Parietal cell hyperplasia
  • Peptic ulcers in SI
29
Q

Consequence of a b-cell tumour in the islets of langerhans?

A

–> Insulinoma
—> Hypoglycaemia
Presents as:
-Confusion
Sweating
Palpitations
Muscle weakness
Blurred vision

30
Q

Consequence of a a-cell tumour in the islets of langerhans?

A 
--> Glucagonoma 
Presentation as..
-Anaemia
-Diabetes
-Necrolytic migratory erythema
31
Q

Consequence of a delta-cell tumour in the islets of langerhans?

A

–> Somatostatinoma

Leads to..

  • Achlorhydria
  • Cholelithiasis
  • Diabetes
  • Steatorrhea
32
Q

MEN?

A

Multiple endocrine neoplasia

** This is a familial syndrome **

MD4001 Week 11 (7 decks)

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