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Key ALS facts > Block 15 > Flashcards

Block 15 Flashcards

1
Q

Definition of Cirrhosis

A

chronic damage → hepatocyte destruction → chronic scarring + damage tht become irreversible → liver becomes fibrotic

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2
Q

Which cells mediate the fibrosis process?

A

Stellate cells

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3
Q

Where are stellate cells found?

A

in the perisinusoidal space btwn. hepatocytes + sinusoid

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4
Q

Main function of stellate cells

A

store vitamin A

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5
Q

What do injured hepatocytes release that activate stellate cells?

A

parakrin factors

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6
Q

What happens to activated stellate cells?

A
  • they lose vitamin A
  • they proliferate
  • they secrete TGF-beta

all of this triggers collagen production => fibrotic tissue formation

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7
Q

Explain the mechanism of portal hypertension

A

build up of fibrotic tissue compresses central vein + sinusoids → increases P in sinusoid and thus the portal veins

OR

new vessels produced in angiogenesis provide low-volume, high P venous drainage tht cannot accomodate as much blood vol as normal => portal vein P increases

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8
Q

Why does portal hypertension increase risk of ascites + congestive splenomegaly?

A

increased chance tht fluid in BVs gets pushed into tissues + across tissues into lrg open spaces e.g. peritoneal activity –> ascites

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9
Q

Pathological effects of decreased liver function

A
  • ⇒ decreased detoxification ⇒ toxins can enter brain and cause hepatic encephalopathy e.g. ammonia → asterixis(hand tremor)
  • decreased oestrogen metabolism ⇒ more oestrogen in blood → gynaecomastia, spider angiomata, palmar erythema
  • increased unconjugated bilirubin as liver normally conjugates bilirubin ⇒ jaundice
  • decreased albumin → hypoabluminaemia
  • decreased clotting factor production- prolongs prothrombin time
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10
Q

Describe some histopathological features of cirrhosis:

A
  • regenerating nodules

- bridging fibrosis

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11
Q

Why does transaminase increase in hepatitis?

A

damaged hepatocytes leak out amino transminase into blood which increases liver transaminase => ALT + AST will increase

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12
Q

Describe the general mechanism of hepatitis infection

A

Hep virus infects hepatocyte → CD8+ cells recognise abnormal proteins presented on MHC I → Cytotoxic killing → hepatocyte apoptosis → liver damage → increased transaminase

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13
Q

What are then signs + symptoms of the icteric phase of acute viral hepatitis?

A
  • darkened urine -> conjugated bilirubin gets filtered into urine making it darker

Jaundice

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14
Q

Anticteric hepatitis is

A

hepatitis w/o jaundice

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15
Q

3 types of jaundice

A

Pre-hepatic

Intrahepatic

Post-hepatic

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16
Q

Pre-hepatic jaunduce

A
  • excessive RBC breakdown

- overwhelms liver’s ability to conjugate bilirubin ⇒ unconjuagted hyperbilirubinaemia

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17
Q

Causes of Intrahepatic Jaundice

A

hepatic cell dysfunction ==> liver loses ability to conjugate bilirubin

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18
Q

Causes of post-hepatic jaundice

A

biliary drainage obstruction

e.g. gallstones, abdo masses

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19
Q

Definition of Jaundice

A

high levels of bilirubin in blood

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20
Q

Most common causes of jaundice

A
  • viral hepatitis

- alcohol related liver disease

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21
Q

Types of hepatitis transmitted by faecal-oral route

A

Hep A and Hep E

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22
Q

Type of hepatitis transmitted by blood

A

Hep C and Hep B

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23
Q

Key marker of Hep B

A

HBV surface antigen HbsAg

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24
Q

Which Hep virus needs Hep B to infect?

A

Hep D

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25
Q

Elevated IgM in Hep A + Hep E infection indicates

A

active infection

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26
Q

How can acute hepatitis be differentiated from other causes of jaundice?

A

marked elevations of AST + ALT

ALT typically higher than AST

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27
Q

Adults at high risk of HBV infection

A
  • Men who have sex with men
  • People with a sexually transmitted infection
  • People who have had > 1 sex partner during the previous 6 months
  • Health care and public safety workers potentially exposed to blood or other infectious body fluids
  • People who currently or have recently injected illicit drugs
  • People who have diabetes and are < 60 years old (or ≥ 60 years if their risk of acquiring HBV is considered increased)
  • People with end-stage renal disease who receive dialysis, HIV infection, or chronic liver disease, or hepatitis C
  • Household contacts and sex partners of people who are HBsAg-positive
  • Clients and staff members of institutions and nonresidential day care facilities for people with developmental disabilities
  • People in correctional facilities or facilities providing services to injection-drug users
  • International travelers to regions with high or intermediate HBV endemicity
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28
Q

4 main types of shock

A

Hypovolaemic - low blood volume; can be haemorrhagic or non-haemorrhagic

Cardiogenic - trauma to heart tht prevents it from pumping oxygenated blood to rest of body

Obstructive - type of cardiogenic shock can be due to obstruction of flow e.g. pulmonary embolus OR restriction of flow -> physical restriction due to fluid in pericardial sac e.g. cardiac tamponade, tension pneumothorax

Distributive - excessive vasodilation → decreases vascular resistance which decreases BP

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29
Q

2 types of hypovolaemic shock

A

Non-haemorrhagic - not from bleeding e.g. dehydration

Haemorrhagic - from bleeding e.g. due to ruptured BVs

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30
Q

Medical definition of shock

A

Failure of the circulation that results in INADEQUATE TISSUE PERFUSION

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31
Q

Mixed venous oxygen saturation

A

=> amount oxygen bound to Hb coming to R side of heart i.e the oxygen not extracted/used by tissues

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32
Q

Most common cause of cardiogenic shock

A

acute MI → muscle cells die → weaker contractility → less blood pumped out of heart

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33
Q

What class of shock is septic shock?

A

Distributive

34
Q

Inheritance

Lynch syndrome is a

A

Autosomal dominant condition caused by mutations in DNA mismatch repair genes that increases your risk of bowel caner

35
Q

Think modifiable, non-modifiable and genetics

Risk factors for bowel cancer

A

Non-modifiable

  • older age
  • male
  • having IBD

Modifiable

  • smoking
  • eating red meat
  • lack of fibre
  • obesity

Genes

  • familial adenomatous polyposis
  • hereditary nonpolyposis (lynch syndrome)
36
Q

Where do most colorectal carcinomas arise?

A

ADENOCARCINOMAS -> from the intestinal glands/crypts

37
Q

Definition

Primary biliary cirrhosis is:

A

chronic disease that affects the bile ducts, leading to blockage, causing the build up of bile within the liver, causing liver inflammation and scarring

38
Q

Acute cholangitis is

A

acute inflammation and infection of the common bile duct due to:

chronic obstruction or bacterial growth

39
Q

Charcot’s triad of symptoms is

A

FEVER

ABDOMINAL PAIN

JAUNDICE

40
Q

Reynolds pentad of symptoms:

A

(first 3 are the same as Charcot’s triad)
FEVER

ABDO PAIN

JAUNDICE

CONFUSION

HYPOTENSION

41
Q

Embryonic origin of adrenal medulla

A

Neural crest ectoderm

42
Q

Embryonic origin of adrenal cortex

A

intermediate mesoderm

43
Q

Where are bile salts/acids reabsorbed?

A

terminal ileum

44
Q

Why can removal of the terminal ileum cause diarrhoea?

A

because bile salts/acids cannot be reabsorbed so they enter the colon + increase electrolyte + water secretion => increases motility ===> diarrhoea

45
Q

Which type of GI cancers usually produces visible bleeding or mucous and are often palpable on digital rectal examination

A

Rectal cancers

46
Q

Malnutrition

A

insufficient dietary intake to meet current metabolic requirements

47
Q

Malabsorption

A

disorder of digestive tract resulting in inability to use an appropriate dietary intake

48
Q

Which group of people are most at risk of Vitamin B12 deficiency?

A

ALCOHOLICS

49
Q

What is the cause of Gilbert syndrome?

A

harmless condition caused by excessive bilirubin due to RBC breakdown

50
Q

Risk factors for acute pancreatitis

A

G- gallstones

E - ethanol

T - trauma

S - steroids (anabolic)
M - mumps

A - autoimmune

S - scorpion venom

H -hyperglycaemia, hypercalcemia

E - ERCP
D - drugs - valproic acid, sulphonamides, azathioprine, oestrogen preparations

51
Q

major androgen secreted by the adrenal gland

A

Dehydroepiandrosterone

52
Q

Which enzyme inactivates the active steroids -> inactive steroids?

A

11 beta-HSD2 dehydrogenase

53
Q

Addison’s disease

Cause of : Primary adrenal insufficiency

A

caused by destruction or dysfunction of the adrenal cortex

54
Q

Cause of Secondary adrenal insufficiency

A

caused by a reduction in adrenocorticotropic hormone release

55
Q

Cause of tertiary adrenal insufficiency

A

caused by a reduction in corticotropin-releasing hormone

56
Q

Acute, life-threatening presentation of Addison’s disease

A

Addinsonian crisis

57
Q

In which type of adrenal insufficiency is an “Addinsonian crisis” most common?

A

Tertiary adrenal insufficiency (due to withdrawal exogenous steroids)

58
Q

Reduction in glucocorticoid + mineralocorticoid hormone production

A

Adrenal insufficiency

59
Q

What is Conn’s syndrome

A

Primary Hyperaldosteronism caused by XS aldosterone independent of the RAAS system

60
Q

What is a Phaeochromocytoma?

A

catecholamine secreting tumour of chromaffin cells

61
Q

Why is prothrombin time a better measure of acute liver failure compared to albumin?

A

because it has a shorter half-life

62
Q

DEFINE

Tenesmus

A

feeling of incomplete evacuation

63
Q

Which zone of the adrenal cortex contains lipofuscin?

A

ZONA RETICULARIS

64
Q

Which zone of the adrenal cortex has secretory cells arranged in cords?

A

Zona fasiculata

65
Q

Which zone in the adrenal cortex has cells arranged in irregular ovoid clusters?

A

ZONA GLOMERULOSA

66
Q

Site of CRH release

A

paraventricular nucleus of hypothalamus

67
Q

When are cortisol levels highest?

A

Morning

68
Q

Most common cause of Addison’s disease (primary adrenal insufficiency)

A

autoimmune adrenalitis

69
Q

Why can excess ACTH cause hyperpigmentation?

A

because it can be cleaved to alpha melanocyte stimulating hormone, bind its R and increases melanin production.

70
Q

What are the effects of glucocorticoid during times of stess?

A

Anti-inflammatory

Immunosuppression

71
Q

Approximately how many litres of food can be absorbed from the small intestine

A

~8.5 L due to its leaky nature

  • so only small amount of material enters the lrg intestine and this is created as faeces
72
Q

Proximal region of the colon (caecum) is connected to the distal ileum by the:

A

ileocaecal valve

73
Q

What two structural mechanisms are there in the rectum to prevent unwanted release of faecal material?

A

Anorectal angle

Anal sphincter which is normally closed

74
Q

Type 5-7 on the bristol stool chart indicates

A

diarrhoea + urgency

75
Q

Type 3-4 on the bristol stool chart indicate

A

normal - easier to pass

76
Q

Type 1-2 on the bristol stool chart indicate

A

constipation

77
Q

Sulphalazine belongs to what drug class

A

Aminosalicylates

78
Q

Which agent may used for prior surgery or investigation of the bowel?

A

Sodium picosulphate/ Bisacodyl => stimulant laxative which decreases water reabsorption, softening faeces

79
Q

Excessive use of laxatives can cause:

A

Melanosis Coli -> pigmentation of lrg intestine

Tolerance

80
Q

Inferior mesenteric vein drains into

A

splenic vein

81
Q

MoA of Loperamide

A

acts on μ-opioid receptors in the myenteric plexus of the large intestine => anti-diarrhoeal

Key ALS facts (6 decks)

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