Block 15 Flashcards

0
Q

What are the main causes of cirrhosis of the liver?

A

Steatosis –> hepatitis –> cirrhosis

Causes of steatosis = alcoholic fatty liver disease + non-alcoholic fatty liver disease

Causes of hepatitis = viral (A, B, C, EBV, HSV, VZV), autoimmune (3 main diseases), metabolic (Wilson’s, haemochromotosis)

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1
Q

What are the main autoimmune diseases of the liver that can cause cirrhosis?

A

Autoimmune hepatitis
Primary sclerosis cholangitis (autoimmune disease of the bile ducts both intra-hepatic and post-hepatic)
Primary biliary sclerosis (autoimmune disease of the small bile canuliculi)

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2
Q

What are the two main features of liver cirrhosis?

A

Fibrosis (usually encircling the lobule)

Nodules (formed from hyperplasia of hepatocytes within the boundaries of fibrosing strictures)

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3
Q

What is a keiser-fletcher ring?

A

A ‘golden halo’ found within the iris of patients with Wilson’s disease, caused by large deposits of copper

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4
Q

What are the major proteins found within the blood?

A

Albumin
Globulin
Fibrinogen

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5
Q

What are the major tests that are part of the liver function panel?

A
Bilirubin 
Albumin
Total protein
Aspartine aminotransferase 
Alanine aminotransferase 
Gamma-glutamyltransferase
Alkaline phosphatase
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6
Q

What do raised AST or ALT mean?

A
AST = non liver specific and found in cardiac and skeletal muscle. 
ALT = is liver specific 

The ratio of ALT to AST can provide insight but complex.
A very high level of these enzymes suggest: drug induced hepatitis, viral hepatitis, ischaemia or autoimmune hepatitis.

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7
Q

Why is albumin not useful as an indicator for acute liver diseases?

A

Has a half life of ~ 20 days

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8
Q

What does a raised GGT suggest?

A

Related to the bile ducts - cholecystitis

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9
Q

What does raised ALP suggest?

A

Comes from the cells lining the bile ducts. Raised with GGT in cholecystitis and other inflammatory diseases of the gall bladder.

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11
Q

What is the relative incidence and death rate of bowel cancer?

A

4th most common cancer (after breast, prostate and lung)

2nd most common cause of cancer death (after lung)

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12
Q

What are the causes of acute pancreatitis?

A
Idiopathic
Gall stones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion bites
Hyperlipidaemia
ERCP
Drugs
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13
Q

What are the 3 main results of septic shock - caused by microbial constituents or inflammatory mediators?

A

Hyper-coagulability
Vasodilation
Increased vascular permeability

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14
Q

What hormones are produced from the anterior pituitary?

A
Thyroid stimulating hormone
Adrenocorticotropic hormone
Leutinizing hormone 
Follicle stimulating hormone
Prolactin
Growth hormone
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15
Q

What hormones are secreted from the posterior pituitary?

A

Oxytocin

Anti-diuretic hormone

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16
Q

What is the action of thyroid stimulating hormone?

What is its control?

A

To promote release of T3 and T4 from the thyroid gland
Increases iodine uptake by the thyroid gland

Controlled by thyrotropin releasing hormone from the hypothalamus. Secretion of TRH is controlled by stress/cold by the CNS.
Inhibited by T3 and T4 levels in the blood

17
Q

What is the action and control of adrenocorticotropic hormone?

A

Acts to release cortisol from the adrenal cortex.
(Celaved from melanocytic hormone and can cause skin pigmentation).

Controlled by CRH from the hypothalamus
Secretion has a diurnal rhythm
CRH is inhibited by negative feedback from blood glucocorticoids.

18
Q

What is the action of LH and FSH?

How are they controlled?

A

Released by the anterior pituitary in response to GnRH from the hypothalamus. GnRH production is regulated by levels of LH and FSH in the blood. However, in females, oestrogen levels cause switch to +ve feedback and sudden rise in LH/FSH to cause ovulation once a month.

Female:
LH = stimulation of ovulation, supports the theca cells to produce testosterone, helps support corpus luteum for first 2 weeks before implantation.
FSH = stimulates granulose cells to produce oestrogen from testosterone.

Male:
LH = acts on the interstitial cells of leydig in the testes to produce testosterone
FSH = acts on the sertoli cells to promote the stimulation of sperm cells.

19
Q

What is the action of prolactin and how is it controlled?

A

Acts on the glandular tissue (lactocytes) of the breast to stimulate milk production.
Also released during pregnancy to help development of the acinar structure of the brest

Stimulated by nervous impulses from suckling at the nipple.

20
Q

What is the action of growth hormone and how is it control eld?

A

Acts on the long bones and soft tissue to cause growth via the release of insulin like growth factors (IGFs).
Essential for growth but growth only occurs if both growth hormone and sufficient nutrients are available.

Insulin like action to promote metabolism and uptake/storage of proteins and fats.

Released from the anterior pituitary in response to GHRH from the hypothalamus. GHRH stimulated by stress and exercise. Particularly released after just after birth and during puberty.

21
Q

What are the two hormones released from the posterior pituitary?

A

Oxytocin

ADH

22
Q

What is the function of oxytocin and how is it controlled?

A

Acts on the uterine myometrium to cause contraction in childbirth
Acts on the myoepithelial cells of the breast to cause ejection of milk.

Stimulated by nervous impulses from both vaginal stretch and nipple suckling.

23
Q

What is the function of ADH and how is it controlled?

A

Acts on the distal convoluted tubule and collecting ducts of the nephron to increase water reabsorption by action on aquaporin 2.

Controlled by blood osmotic pressure via osmoreceptors in the hypothalamus.

24
Q

What are the possible consequences of a pituitary adenoma?

A

Increased growth hormone release

Increased ACTH release

Increased LH/FSH release

Increased TSH release

25
Q

What are the broad causes of oedema?

A

Reduced plasma oncotic pressure = liver failure, nephrotic, kwashiorkor

Lymphatic obstruction = lymphodema, tumor

Increased hydrostatic pressure = congestive heart failure, portal hypertension

Increased endothelial permeability = inflammation

Increased interstitial Na+ = hyperaldosteronism

26
Q

What inflammatory mediators are involved in acute inflammation?

A
Bradykinins 
Prostaglandins (E2)
Interleukins (IL1, IL6, TNF)
Histamine
Serotonin
27
Q

Histamine (production and action)

A

Mast cells in acute inflammation

Vasodilation and increased vascular permeability

28
Q

Serotonin (production and action)

A

Platelets

Vasodilation and increased vascular permeability

29
Q

Bradykinin (production and action)

A

Activated factor 12 cleaves:
prekallikrein –> kallikrein
Kallikrein cleaves:
kininogen –> bradykinin

Increase vascular permeability, pain, vasodilation, bronchoconstriction

30
Q

What are the main prostaglandins and their action?

A

Thromboxane A2 = platelet aggregation and vasoconstriction

PgI2 = vasodilation and platelet inhibition

PgE2 = pain, vasodilation, (widely found in the body, smooth muscle constriction and relaxation), hypothalamus to raise temperature set point

31
Q

What are the main interleukins and their action?

A
IL-1 = induces inflammatory response
IL-2 = clonal expansion of T-cells
IL-4 = B-cell stimulation
IL-6 = B-cell differentiation
IL-8 = enhances inflammation via chemotaxis
IL-12 = promotes immune response.
32
Q

What are the stages of shock?

A

Compensated = perfusion maintained by: increased cardiac output, vascular resistance, RAAS

Decompensated = progressive decrease in tissue perfusion

Irreversible = Irreversible tissue injury and organ failure