EXAM REVISION Flashcards
(39 cards)
What is the pathophys of T1DM?
An autoimmune condition where the body attacks the insulin producing beta cells that are found in the pancreas. This leads to a lack of insulin production and then creates an elevated BGL - hyperglycaemia.
What is the pathophys of T2DM?
A condition characterised by insulin resistance, where the body’s cells become less responsive to insulin and beta cell dysfunctions, leading to decreased insulin secretion. The pancreas tries to produce more insulin however it is not a sufficient amount and over time this leads to hyperglycaemia. Associated with lifestyle and diet.
Pathophys of DKA?
Occurs due to severe insulin deficiency, seen in T1DM. Glucose cannot enter the cells which leads to increased lipolysis (fat breakdown). This then produces ketones as the body is trying to use fat for fuel. An accumulation of ketones causes metabolic acidosis and has symptoms including polyuria, dehydration, kussmaul respirations, fruity break, altered mental status
pathophys of Hyperosmolar hyperglycaemic state (HHS)?
A case of extreme hyperglycaemia seen in T2DM without significant ketone production. Insulin levels are inadequate to use glucose effectively but sufficient enough to prevent lipolysis and ketosis. This severity causes osmotic diuresis leading to significant dehydration and electrolyte imbalances. Symptoms extreme thirst, polyuria, confusion and lethargy.
What is a chronic complication of T2DM and what does it do?
Chronic hyperglycaemia leads to the damage of blood vessels.
Microvascular complications: damage to retinal blood vessels, nephropathy (glomerular damage), neuropathy (nerve damage due to ischemia and hyperglycaemia)
Macro vascular complications: increased risk of cardiovascular disease, coronary artery disease, cerebrovascular disease and peripheral artery disease due to accelerated atherosclerosis.
What is the relationship between serum potassium and insulin administration?
Insulin promotes the uptake of potassium into cells by activating the sodium potassium ATPase pumps. This can lead to lower serum potassium levels (hypokalemia). This is relevant when we are administering insulin therapy to a DKA or HHS pt, where insulin can rapidly shift potassium into the cells.
What is the pathophysiology of renal failure and some signs and symptoms?
This is a sudden loss of kidney function from hours to days, which leads to the accumulation of waste products left in the body, fluid imbalances, and electrolyte disturbances. Categorised into 3 groups:
Pre-renal failure - decreased blood flow to kidneys. Low perfusion leads to low glomerular filtration rate and urinary output. Symptoms include hypotension, tachycardia, dry mucous membranes
Intrinsic renal failure — results from direct damage to kidneys tissue. Damaged nephrons cause lowered filtration rate and reabsorption capabilities. Symptoms include fatigue, nausea, confusion, oluguria, oedema.
Post-renal failure - caused by an obstruction to urine flow, such as kidney stones or tumours. Leads to higher pressure in the renal tubules and lowered GFR. Symptoms include Liguria or anuria, lower abdominal pain.
Pathophysiology of chronic kidney disease (CKD) and signs and symptoms
CKD is a progressive and irreversible loss of kidney function over months to years. The kidneys have an impaired ability of filtering out waste, regulating fluid balance and maintaining electrolyte/acid base balance. Symptoms include cardiovascular complications, anaemia, bone and mineral disorder, uremic syndrome, fluid/electrolyte imbalances
Pathophysiology of acid based imbalance that can occur with kidney injury
Metabolic acidosis in kidney injuries occurs when the kidneys are unable to excrete a sufficient amount of hydrogen ions (H+) or reabsorb bicarbonate, which helps maintain blood pH levels within normal ranges (7.35-7.45). Signs and symptoms include kussmaul breathing, fatigue and weakness, confusion, nausea and vomiting.
What is hypernatremia?
An elevated level of sodium in the body which can lead to hyperosmolality which affects the water movement between intra and extra cellular spaces = cellular dehydration
What are the neurological symptoms of hypernatremia?
When sodium is high, extracellular fluid become HYPOtonic compared to the intracellular fluid. The water moves from our brain cells to the extracellular space to balance out the osmolality, which leads to cell dehydration causing dysfunction.
How do we manage hypernatremia with IV fluids?
Administer a HYPOtonic fluid such as 0.45% saline or 5% dextrose in water SLOWLY to avoid rapid shift in water, which can lead to cerebral oedema. These fluids are used in this case as they have a lower osmolality rate than blood and that assists with gradually lowering sodium levels and rehydrating the cells.
What is an ABG analysis?
This is used to diagnose and assess acid based imbalances by looking at the oh, partial pressure of carbon dioxide (PaCO2) and bicarbonate (HCO3-)
What is respiratory acidosis?
Occurs when there is HYPOventilation, leading to retention of CO2 (increased PACO2). It increases the formation of carbonic acid, lower the blood sugar level to under 7.35. Common causes are COPD severe asthma, and drug overdose. It is compensated by the kidneys raising HCO3- reabsorption, to buffer the risen CO2.
What is respiratory alkalosis?
Occurs when there is HYPERventilation leading to the loss of CO2therefor the blood pH is risen. Common causes are anxiety, pain, high altitude, conditions that stimulate respiratory centre. Compensated by kidneys lowering HCO3- to get the pH back down to normal ranges.
What is metabolic acidosis?
An excess of acid and loss of bicarbonate, meaning lower HCO3- and a pH under 7.35 (acidic). Common causes are DKA, lactic acidosis, renal failure, diarrhoea. Can be compensated by the lungs increasing ventilation to blow off CO2 (kussmaul respirations) and raise the pH
What is metabolic alkalosis?
An excess of bicarbonate and loss of hydrogen ions (H+) leading to elevated blood pH. Common causes are vomiting, diuretic use, excessive bicarbonate intake. Can be compensated by lungs decreasing ventilation to retain CO2 therefore lower pH.
Which organs are responsible for acid-base balance?
The lungs and kidney. The lungs are for short term regulation, their role being to regulate blood pH through control of the CO2 levels. Changes in the RR can rapidly adjust the amount of CO2 exhales, therefore altering levels of carbonic acid in the blood. This occurs within minutes/hours
The kidneys are for long term regulation, their role is to maintain by reabsorbing HCO3- and excreting H+. This helps to maintain a balance pH over a period of hours to days.
Pathophysiology of alcoholic liver cirrhosis
The final stage of chronic liver disease from prolonged alcohol abuse. This involved irreversible scarring and fibrosis of the liver. The pathophysiological process includes chronic inflammation and injury, fibrosis formation, modular regeneration and cirrhosis, loss of liver function.
Pathophysiology of ascites
The accumulation of fluid in the peritoneal cavity. This results from portal hypertension, increases hydrostatic pressure into the livers portal vein. The pressure builds up because scar tissue restricts the normal blood flow to organs. As the liver dies, it produces less albumin (a protein that maintains oncotic pressure). Lowered albumin reduces this pressure, allowing for fluid to leak from the blood vessels. RAAS activation - the blood volume from fluid shifting into the abdominal space triggers the renin-angiotensin-aldosterone-system, leading to sodium and water retention, contributing to fluid build up in the peritoneal cavity.
Pathophysiology of esophageal varices
This develops as a consequence of portal hypotension. Higher pressure in the portal venous system forces blood to reroute via smaller and less resistant veins. Veins then become engorged and dilated, forming varices. This can lead to life threatening haemorrhage
Pathophysiology of jaundice
An accumulation of bilirubin in the blood causing yellowing of the skin and eyes. The liver is supposed to excrete bilirubin as bile, however in liver failure, hepatocyte damage and impaired bile flow reduce the livers ability to conjugate and excrete bilirubin.
Pathophysiology of hepatic encephalopathy
This is na neurological disorder that occurs in patients with severe liver dysfunction. The liver cannot detoxify substances from the blood, leading to an accumulation of neurotoxicity substances such as AMMONIA - the most toxic substance to the brain. Symptoms can include confusion, disorientation, and altered level of consciousness.
What is the most toxic substance to the brain and why
Ammonia as is disrupts energy production, imbalances neurotransmitters, causes brain oedema and it can cross the blood brain barrier
