- PATHOPHYSIOLOGIES - Flashcards
Outline the pathophysiology of DKA
A hyperglycaemic syndrome resulting in severe:
- Acidosis
- Dehydration
- Electrolyte imbalance (Na+, K+, glucose)
- Autoimmune attack on B cells in the pancreas causing a decrease in insulin production
- Lack of insulin increases gluconeogenesis and glycogenolysis and a decrease in glycolosis
- This all together results in an increased amount of glucose in the bloodstream (hyperglycaemia)
- This results in Glucosuria, Polyuria, and polydipsia
- Lack of insulin production also results in the breakdown of fats (lipolysis)
- the fats are broken down from adipose tissue to form free fatty acids
- These FFA go to the liver and undergo ketogenesis to make more ketone bodies
- This is to obtain a second energy source as glucose is not working or not present in this case
- This results in a high amount of ketones in the blood (hyperketonaemia) and thus ketones in the urine (ketonuria)
- Ketones are acidic and reduce the pH of the blood and the urine
Outline the pathophysiology of Shock
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Outline the pathophysiology of AKI
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Outline the pathophysiology of CKD
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Outline the pathophysiology of Neurogenic shock
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Outline the pathophysiology of Hypovolaemic shock
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Outline the pathophysiology of Distributive shock
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Outline the pathophysiology of Cardiogenic shock
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Outline the pathophysiology of Heart failure
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Outline the pathophysiology of Asthma
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Outline the pathophysiology of Bronchiolitis
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Outline the Pathophysiology of Croup
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Outline the Pathophysiology of Acute Rheumatic Fever
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Outline the Pathophysiology of Pre-renal causes of AKI
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Outline the Pathophysiology of Intra-renal causes of AKI
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Outline the Pathophysiology of Post-renal causes of AKI
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Outline the Pathophysiology of Rhabdomyolysis
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Outline the Pathophysiology of the RAAS
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Outline the role of ADH
- ADH is made in the hypothalamus and stored in the pituitary gland
- The stimuli for release of ADH are:
- low blood pressure (presence of angiotensin II, from RAAS pathway)
- high plasma osmolality (blood is hypertonic, low amount of water in the blood and high solutes) - osmoreceptors on the hypothalamus are stimulated by high plasmaosmolality, and there are also receptors for angiotensin II
- This stimulates the release of ADH
- ADH travels to the kidneys and acts on the cells in the collecting duct by binding to vasopressor receptors
- This activates an intracellular cascade that results in the activation of Protein kinase A
- PKA stimulates Aquaporin II protein channels to fuse with the cell membrane absorb water from the filtrate that otherwise would have been secreted
- This water travels into the cell and into the blood stream via Aquaporin III and IV channels
- This incease in water in the blood stream causes and increase the plasma volume and thus blood pressure and also decreases the osmolality of the blood
- ADH can also bind onto the vasopressin receptors of the smooth muscle cells of the blood vessel
- Stimulating the GQ mechanism resulting in high amounts of calcium, causing the cell to contract -> vasoconstriction -> increase in peripheral resistance -> increase in blood pressure
Discuss the pathophysiology of Type 1 DM
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Discuss the pathophysiology of Type 2 DM
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Discuss the pathophysiology of Hyperosmolar hyperglycaemic non-ketotic syndrome (HHNS)
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Discuss the pathophysiology of Hypoglycaemia
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Discuss the pathophysiology of Type 1 respiratory disorders
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Discuss the pathophysiology of Type II respiratory disrders
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