Flashcards in OSCE Deck (159)
What is acute kidney injury?
-Significant decline in renal function over hours or days manifesting as an abrupt and sustained increase in serum urea and creatinine
What are pre-renal causes of AKI?
-Renalvascular compromise eg NSAIDs, ACE I, renal artery stenosis
Give the main causes of renal AKI
-Acute tubulonecrosis caused by ischeamia, hypertension, thrombotic thrombocytopenia purpura
-Interstitial nephritis by drugs (NSAIDs, Abx) and toxins
Post Renal causes of AKI
-Stones, neoplasm, stricture, prostate
Describe some possible clinical signs of an AKI
-Raised Urea, creatinine, low urine output, acidosis/hyperkalaemia
What investigations would you do in AKI?
-Bloods -> FBCs, U+Es, LFTs, glucose, Ca, clotting, ESR
-ABG to look for acidosis, hypoxia and hyperkalaemia
-ECG, CXR and renal US
Describe the ECG features in order of hyperkalaemia
-Peaked T waves
-Flattened P waves
-Increased PR interval
Describe the stages of alcoholic liver disease. At what stage is it irreversible?
-Fatty liver -> hepatitis -> cirrhosis
Which liver enzymes are commonly raised in alcoholic liver disease?
What is liver cirrhosis?
-Hepatocellular damage producing areas of nodular regeneration separated by fibrous septae
List some clinical signs of Alcoholic liver disease
- Hands -> Clubbing, leuconychia (low albumin), dupytens contracture, palmar erythema,
-Face -> pallor (ACD)
-Trunk -> Spider naevi, gynaecomastia (decreased liver metabolism)
-Abdo -> hepatosplenomegaly, caput medusa, ascites
-General -> jaundice, bruising (coagulopathy), anorexia
What is portal hypertension? Describe the main features
-Raised portal blood pressure >20mmHg
-SAVE (splenomegaly, ascites, varices (oesophageal, caput medusa, worsening piles) and encephalopathy
Describe portosystemic shunting in portal hypertension. Give the vessels involved in all 3 varices
-Raised portal pressure causes a backflow and increased pressure of blood as blood cannot enter portal system. portal vessels become engorged and dilated causing shifting of blood from the portal system into the systemic system.
-Oesophageal -> Left gastric vein to inferior oesophageal veins
-Caput medusa -> peri-umbilical to superficial abdo
-Haemorrhoids -> superficial rectal to inferior/middle rectal
What can be confused for caput medusa on the abdomen and how do you tell these apart?
-blood flow down below umbilicus = portal hypertension
-Blood flow up below umbilicus = ivc obstruction
Why does portal hypertension cause encephalopathy?
-Decreased blood flow through liver decreases detoxification of blood.
-Build up of toxins in systemic system including ammonia ->cross bbb -> astrocytes clear causing glutamate to glutamine -> osmotic imbalance -> cerebral oedema
Describe the pathophysiology of ascites in liver disease
-Back pressure due to accumulation of blood causes increased hydrostatic pressure leading to fluid exudation. This causes a decrease in circulating volume and RAAS activation which enters a cycle of increased exudation and further RAAS activation. Also decreased albumin and impaired aldosterone metabolism
In broad terms what is anaemia? What general symptoms/signs does it produce?
-Decreased capacity of the haemoglobin to carry oxygen
-Fatigue, pallor, palpitations, light headedness
What are the causes of microcytic anaemia?
-Anaemia of chronic disease
-Iron deficiency Anaemia
Describe causes of normocytic anaemia
-Recent blood loss
-Bone marrow failure
What are causes of macrocytic anaemia?
-Vit B12 deficiency
Give some causes of haemolytic anaemia
-Destruction by mechanical heart valves
Give 3 differentials for causes of iron deficiency anaemia
Give 2 signs specific for iron deficiency anaemia
What are the causes of b12 deficiency?
-Bacterial overgrowth syndrome (increased use of b12)
What are the causes of folate deficiency?
What are the specific symptoms in b12 deficiency?
Describe the pathophysiology of asthma
-Bronchial hypersensitivity causing an exaggerated response to normally non-allergenic non-noxious stimuli resulting in mucosal oedema, mucus hypersecretion and bronchoconstriction which leads to reversible airway narrowing. Over time this lead to goblet cell hyperplasia, smooth muscle hypertrophy and airway remodelling .
What cellular/immune components are involved in asthma
-Histamine release from mast cells
-IgE and eosinophils
Name some precipitants of asthma
-Atopy -> t1 hypersensitivity to dust, pollen, animals
-Stress -> cold air, viral urti, exercise, emotion
-Toxins -> smoking, hairspray