Flashcards in Review of posters 28/04/2016 Deck (44):
Alcoholic liver disease pathophysiology
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.
Function of stellate cells in alcoholic liver disease.
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.
How do caput medusae occur?
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.
Signs and symptoms of alcoholic liver disease.
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.
Diagnosis of alcoholic liver disease
Elevated serum bilirubin
" "Serum AST and ALT increased
" "Low Serum albumin
" "Serum alkaline phosphatase.
Types of heart failure?
Left, right, diastolic, systolic
What is systolic heart failure?
Pumping issue- heart muscle is smaller and weaker
What is diastolic heart failure?
Filling issue- heart muscle size gets larger taking up more room.
Left sided heart failure or right sided heart failure?
Left-backs up to the lungs-pulmonary oedema
Right- backs up to the body-peripheral oedema
Causes of heart failure
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.
Treatment of heart failure
Beta blockers/Calcium channel blockers.
Diuretics- loop e.g. furosemide
Lifestyle changes e.g. quitting smoking, exercising, healthy diet, decreasing alcohol intake.
Classes of heart failure
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.
Where does coeliac disease effect?
Upper small bowel
What age group does coeliac disease usually present in?
Middle aged females
Diagnosis of coeliac disease?
Serology- endomysal test
Blood tests- FBC shows anaemia
Describe intermittent claudication.
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.
Treatment of peripheral arterial disease
Aspirin, clopidogrel, hypertension drugs where suitable
6Ps of critical limb ischaemia
pain- first sign
Parathesia- sensory, touch
Pallor- no edema
Pulses-diminished or absent
Paralysis- lack of movement of muscle
Other symptoms of critical limb ischaemia
Absence of peripheral pulses
Treatment of CLI
angioplasty/stenting, surgical reconstruction, amputation
Langerhans cell histiocytes
Proliferation of langerhans cells
Presence of birbeck granules
Caused by smoking
Young kids- unifocal bone lesions, old kids- wide spread symptoms
Treatment of LCH
Cessation of smoking
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
Describe the process of vomiting.
Peristalsis ceases (slow wave is supsended).
Retrogade contraction begins
Epiglottis closes over trachea
Lower oesophageal sphincter relaxes
Strong contraction of the diaphragm-causes vomitus to move up the oesophagus into the mouth
How is vomiting caused
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.
Vagal afferents cause in vomiting
Oesophageal shortening, smooth muscle contraction and retrograde conduction.
Somatic efferents cause in vomiting
Increase HR, increase sweating, increase saliva production and constriction of anal and bladder sphincters
Somatic motor cause in vomiting
Somatic motor cause abdominal muscle contraction and diaphragm contraction
What is the slow wave?
Rhythmic patterns of membrane depolarisation and repolarisation. Electrical signal causing contraction of the muscle cells. Created at the interstitial cells of Cajul- pacemakers.
Where are the interstitial cells of cajul found?
Between longitudinal muscles and circular muscles
What is HCl's role?
Activates pepsinogen to form pepsin
What is Pepsinogen's role?
Activate to form pepsin- autocatalyst. Production of pepsin activates more pepsinogen to become pepsin.
What is Intrinsic factors role?
Binds vitamin B12 so it can be absorbed in the terminal ileum.
What is Gastrin's role?
Activate parietal cells to release HCl
What is somatostatin's role?
Suppress parasympathetic stimulation to inhibit HCl release
What is histamines role?
How is the stomachs mucosa protected?
Secretion of mucus from fovealar cells
What does the mucin contain?
Bicarbonate ions, hydrophobic monolayer, prostaglandins (reduce acid secretion), elimination of H+ in favour of Na_
How do proton pump inhibitors work?
Block by covalent modification directly onto parietal cells.
How do histamine receptor antagonists work? Give an example.
Block competitively on ECL cells preventing them from releasing histamine.
How do muscurinic receptor antagonists work? Give an example.
Block competitively on parietal cells.
Why do NSAIDs cause ulcers
Inhibit prostaglandin secretion via COX1 and COX2 inhibition- therefore acid production will be increased.
What controls stomach emptying?
Distension and stretch of the stomach
Release of gastrin
Increase vagal activity