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Posters > Review of posters 28/04/2016 > Flashcards

Review of posters 28/04/2016 Flashcards

1
Q

Alcoholic liver disease pathophysiology

A

Alcohol is a solvent. It won’t completely dissolve the lipid bilayer however it will make it more liquid. Therefore integral proteins in the lipid bilayer slip out which can lead to inflammation and eventually fibrosis.
Alcohol dehydrogenase system converts alcohol to aldehyde by converting NAD to NADH. This process supresses gluconeogenesis. This causes the liver to increase fatty acid production. Chronic alcohol consumption will chronically suppress gluconeogenesis and therefore fatty acid deposits are left in the Space of Disse. Stimulates Kupffner cells which leads to inflammation.
When the ADS becomes overwhelmed, alcohol is metabolised by secondary pathways which produce a large amount of free radicals which damage the liver.

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2
Q

Function of stellate cells in alcoholic liver disease.

A

Normally store vitamin A. However activated by cytokines to act as hyperactive fibrin depositing cells. Occurs in Space of Disse. (means the hepatocytes no longer have access to nutrients and die off.

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3
Q

How do caput medusae occur?

A

In liver cirrhosis- the Space of Disse gets bigger and thicker due to scar tissue forming, this narrows the sinusoidal lumen and therefore increases the pressure. This pressure backs up to the portal system.

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4
Q

Signs and symptoms of alcoholic liver disease.

A

Hepatomegaly
Often general GI symptoms associated with alcohol intake such as diarrhoea, vomiting.
Patient could be asymptomatic
Occasional mild jaundice
Severe cases would show severe jaundice, ascites, abdominal pain, fever.

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5
Q

Diagnosis of alcoholic liver disease

A

Elevated serum bilirubin
“ “Serum AST and ALT increased
“ “Low Serum albumin
“ “Serum alkaline phosphatase.

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6
Q

Types of heart failure?

A

Left, right, diastolic, systolic

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7
Q

What is systolic heart failure?

A

Pumping issue- heart muscle is smaller and weaker

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8
Q

What is diastolic heart failure?

A

Filling issue- heart muscle size gets larger taking up more room.

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9
Q

Left sided heart failure or right sided heart failure?

A

Left-backs up to the lungs-pulmonary oedema

Right- backs up to the body-peripheral oedema

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10
Q

Causes of heart failure

A

Heart muscle disease-cardiomyopathy
Ischaemia- coronary artery disease
Decreased force of contraction
Valvular disease- (regurgitation means the blood flows backwards- the heart has to work harder and therefore needs more O2 but it can’t get it- therefore the heart muscle dies.

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11
Q

Treatment of heart failure

A

Beta blockers/Calcium channel blockers.
Diuretics- loop e.g. furosemide
ACE inhibitors
Spiranolactone

Lifestyle changes e.g. quitting smoking, exercising, healthy diet, decreasing alcohol intake.

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12
Q

Classes of heart failure

A

Class I- no symptoms at rest or on exercise
Class II- no symptoms at rest- mild limitation on exercise
Class III- no symptoms at rest- gentle physical activity induces symptoms
Class IV- symptoms at rest and on exercise.

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13
Q

Where does coeliac disease effect?

A

Upper small bowel

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14
Q

What age group does coeliac disease usually present in?

A

Middle aged females

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15
Q

Diagnosis of coeliac disease?

A

Serology- endomysal test
-anti-tissue-transglutaminase antibodies
Blood tests- FBC shows anaemia
Bowel biopsy

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16
Q

Describe intermittent claudication.

A

On exercise- muscle demand gets higher- but due to the athersclerotic plaque in the leg- the demands can’t be met and therefore the tissues become ischaemic.

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17
Q

Treatment of peripheral arterial disease

A

Aspirin, clopidogrel, hypertension drugs where suitable

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18
Q

6Ps of critical limb ischaemia

A 
pain- first sign
Parathesia- sensory, touch
Pallor- no edema
Pulses-diminished or absent
Poikothermia- cold
Paralysis- lack of movement of muscle
19
Q

Other symptoms of critical limb ischaemia

A 
Absence of peripheral pulses
Cold
Hairless
Shiny skin
Thick nails
Pulseless
Ulcers
Gangrene
20
Q

Treatment of CLI

A

angioplasty/stenting, surgical reconstruction, amputation

21
Q

Langerhans cell histiocytes

A

Proliferation of langerhans cells
Presence of birbeck granules
Caused by smoking
Young kids- unifocal bone lesions, old kids- wide spread symptoms

22
Q

Treatment of LCH

A

Corticosteroids
Cessation of smoking
Immunosupressive therapy.

23
Q

Goodpastures syndrome

A

Presents initially as upper resp tract infection.
Progresses on to recurrent haemoptysis and eventually anaemia.
Its a type II cytotoxic reaction that can result in intrapulmonary heamorrhage and then acute glomerulanephritis

24
Q

Describe the process of vomiting.

A

Peristalsis ceases (slow wave is supsended).
Retrogade contraction begins
Epiglottis closes over trachea
Breathing ceases
Saliva produced
Lower oesophageal sphincter relaxes
Strong contraction of the diaphragm-causes vomitus to move up the oesophagus into the mouth

25
Q

How is vomiting caused

A

Toxic substances stimulate 5-HT receptors on ECl cells in the stomach. This stimulates sensory afferent neurones in the mucosa to the brainstem. The signals arrive at the nucleus tractus solitares and the chemoreceptor trigger zone. From here impulses are sent to the vomiting centre where vomiting is co-ordinated.

26
Q

Vagal afferents cause in vomiting

A

Oesophageal shortening, smooth muscle contraction and retrograde conduction.

27
Q

Somatic efferents cause in vomiting

A

Increase HR, increase sweating, increase saliva production and constriction of anal and bladder sphincters

28
Q

Somatic motor cause in vomiting

A

Somatic motor cause abdominal muscle contraction and diaphragm contraction

29
Q

What is the slow wave?

A

Rhythmic patterns of membrane depolarisation and repolarisation. Electrical signal causing contraction of the muscle cells. Created at the interstitial cells of Cajul- pacemakers.

30
Q

Where are the interstitial cells of cajul found?

A

Between longitudinal muscles and circular muscles

31
Q

What is HCl’s role?

A

kills micro-organisms
Activates pepsinogen to form pepsin
Denatures protein

32
Q

What is Pepsinogen’s role?

A

Activate to form pepsin- autocatalyst. Production of pepsin activates more pepsinogen to become pepsin.

33
Q

What is Intrinsic factors role?

A

Binds vitamin B12 so it can be absorbed in the terminal ileum.

34
Q

What is Gastrin’s role?

A

Activate parietal cells to release HCl

35
Q

What is somatostatin’s role?

A

Suppress parasympathetic stimulation to inhibit HCl release

36
Q

What is histamines role?

A

Stimulates HCl

37
Q

How is the stomachs mucosa protected?

A

Secretion of mucus from fovealar cells

38
Q

What does the mucin contain?

A

Bicarbonate ions, hydrophobic monolayer, prostaglandins (reduce acid secretion), elimination of H+ in favour of Na_

39
Q

How do proton pump inhibitors work?

A

Block by covalent modification directly onto parietal cells.

40
Q

How do histamine receptor antagonists work? Give an example.

A

Rantididine

Block competitively on ECL cells preventing them from releasing histamine.

41
Q

How do muscurinic receptor antagonists work? Give an example.

A

Pirezipine

Block competitively on parietal cells.

42
Q

Why do NSAIDs cause ulcers

A

Inhibit prostaglandin secretion via COX1 and COX2 inhibition- therefore acid production will be increased.

43
Q

What controls stomach emptying?

A

Distension and stretch of the stomach
Release of gastrin
Increase vagal activity

44
Q

How can the duodenum delay chyme release?

A

Release of CCK and enterogastrin from enteroendocrine cells. Causes contractile force of stomach to decrease.
Fat in the lumen- needs to be absorbed before.
Acid in the duodenum- needs to be supressed before arrival of more acidic chyme.

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