Exam Prep

Question 1

Hyperaldosteronism

Answer 1

Excessive aldosterone secretion by the adrenal cortex.
CM: sodium retention, hypertension, increased potassium excretion.
Treatment: Correction of underlying causes, management of hypertension and hypokalaemia, aldosterone antagonists such as spironolactone

Question 2

T1DM

Answer 2

The complete destruction of islet cells of the pancreas and little to no insulin production.
Insulin-dependent.
Prone to hypoglycaemia and ketoacidosis
Results from a lack of insulin caused by loss of beta cells (Related to genetic susceptibility, autoimmunity and environmental factors)
CM: Affected metabolism of protein and carbs, hyperglycaemia, glycosuria. Acute presentation is polyphagia, polyuria and polydipsia
Treatment: Insulin, meal planning, exercise. Pancreatic transplant in extreme cases

Question 3

T2DM

Answer 3

Insulin resistance at the target cells
May progress to insufficient pancreatic insulin release and islet cell destruction
Initially, insulin secretion by the pancreas is increased, resulting in hyperinsulinaemia. Over time, excessive production of insulin leads to the fatigue of the pancreatic beta cells (that produce insulin), which then leads to cells being unable to produce insulin
Generally occurs in those over 35 y/o, strongly related to obesity.
Onset is insidious with non-specific symptoms, making early diagnosis difficult (fatigue, recurrent infection)
Treatment: Oral agents, progressing to insulin treatment

Question 4

DM: Pharmacological treatment

Answer 4

Metformin: first-line treatment for type 2, most commonly used. Increases glucose uptake and usage at target tissues
Sulfonylureas (e.g. glicazide): Traditionally used as second-line agents. Act on the pancreatic beta cells to increase secretion of insulin and also increase the response to insulin at the target tissues

Question 5

Hypoglycaemia

Answer 5

BGL below 4 mmol/L.
Caused by insulin excess, over-exercising and inadequate carbohydrate intake. If the level drops to 2.5 mmol/L and remains untreated, it will be a medical emergency and can progress to brain damage, seizures, coma and death
Treatment is the immediate replacement of glucose through quick-acting carbs, then later long acting carbs.

Question 6

Hyperglycaemia

Answer 6

BGL above 15mmol/L.
Caused by poor diabetic control - insufficient insulin, certain drugs (glucocorticoids), increase in the insulin counter-regulatory hormones (adrenaline, cortisol)
Treatment: Insulin, oral hypoglycaemic agents

Question 7

Diabetic Ketoacidosis (DKA) overview

Answer 7

Common T1 complication characterised by extreme hyperglycaemia. Usually occurs following a stress such as infection, or omission of insulin. It is a serious medical emergency that, if untreated, can lead to coma and death

Question 8

DKA: Pathophysiology

Answer 8

• Deficiency of insulin: leads to the breakdown of fat stores to be used as energy instead of glucose.
• Increased insulin-resistant cells: The inability of glucose to enter cells can lead to the usage of lipids as cell fuel instead of glucose.
  The breakdown of fat stores means:
  
  • Ketones are released as a result of the fat breakdown.
  • Ketones are acidic > result in ketoacidosis
  • Will show high levels of ketones in the urine

Question 9

DKA: Symptoms

Answer 9

Acetone breath (smells sweet and fruity), increased respiratory rate, thirst (due to dehydration)

Question 10

DKA: Treatment

Answer 10

Insulin replacement (priority), fluids to correct dehydration, bicarbonate may be used to lessen the acidosis

Question 11

Hyperglycaemic hyperosmolar state (HHS): Pathophysiology

Answer 11

Uncommon but significant complication of T2 with high overall mortality. Characterised by:
- High levels of serum glucose (more than 30 mmol/L), the osmolarity of blood becomes high, due to high glucose levels and low water levels, leading to intracellular fluids moving to intravascular fluids.
- This leads to severe dehydration; large amounts of glucose excreted into urine > water drawn together > hypovolaemia and hypotension.
- Risk factors are elderly individuals, comorbidities such as infections, cardiovascular disease or renal disease.

Question 12

HHS treatment

Answer 12

IV saline, IV insulin and correction of hypokalaemia

Question 13

Chronic complications of diabetes

Answer 13

CVD, Stroke, Diabetic retinopathy, Diabetic neuropathy

Question 14

CVD (complication)

Answer 14

Due to atherosclerosis. Insulin resistance and insufficient insulin lead to altered lipid metabolism. Low HDL plus elevated triglycerides and low-density lipoproteins (LDL, atherosclerosis increases)

Question 15

Stroke (complication)

Answer 15

Atherosclerosis and accompanying hypertension increase risk

Question 16

Diabetic retinopathy (complication)

Answer 16

Changes to the retinal blood vessels that can cause them to haemorrhage or leak fluid

Question 17

Diabetic neuropathy (complication)

Answer 17

Affects all peripheral nerves including pain fibres and the autonomic nervous system

Question 18

Hyperthyroidism

Answer 18

• A condition where thyroid hormone levels are higher than normal.
• Clinical manifestations: Tachycardia, nervousness, insomnia, heat intolerance, weight loss
• The most common cause is Graves’ disease

Question 19

Hypothyroidism

Answer 19

• Deficient production of thyroid hormone
• Clinical manifestations: Lower energy metabolism, lower heat production, delays neuromuscular processes within the body. Results in lethargy, tiredness, constipation
• Treatment: Hormone replacement therapy, Thyroxine needs to be taken separately from food, vitamins and mineral supplements to ensure adequate absorption

Question 20

UTI

Answer 20

• An inflammation of the urinary epithelium usually caused by bacteria from gut flora. Can occur anywhere along the urinary tract: urethra, prostate, bladder, ureter or kidney
  
  • Mechanisms to protect against UTIs: Most bacteria is washed out of the urethra during urination. Low pH causes a bactericidal effect, which is why it is important to pass urine after sexual activity
  • Risk factors: Premature newborns, pre-pubertal children, cystitis more common in women due to shorter urethra and closeness of urethra to anus (increased possibility of bacterial contamination from the intestines)

Question 21

Acute cystitis

Answer 21

• Inflammation of the bladder, often caused by infecting microorganisms. Usually caused by retrograde movement of bacteria into the urethra to the bladder
  
  • Often asymptomatic, but symptoms may include dysuria, low back pain, urgency and frequency of urination. Evaluated by urine dipstick testing or urine culture from freshly voided urine
  • Treatment: Microorganism-specific antibiotic

Question 22

Acute pyelonephritis

Answer 22

• Inflammation of the renal pelvis and interstitium, often caused by infection. The most common risk factors are urinary obstruction and reflux of urine from the bladder. Causes renal inflammation, renal oedema and purulent urine (containing pus)
  
  • Symptoms: Acute onset fever, chills and flank or groin pain. Frequency, dysuria and flank tenderness.
  • Evaluation and treatment: Urine culture, urinalysis and clinical signs and symptoms. Antibiotic therapy use

Question 23

Glomerulonephritis

Answer 23

• Inflammation of the glomerulus. Can show proteinuria and haematuria. Risk factors include immunological abnormalities (the most common cause), drugs, toxins, infection and diabetes.
  
  • Treatment depends on the management of the cause; antibiotics, diet changes, immunosuppressants

Question 24

Acute kidney disease (AKD)

Answer 24

Refers to a sudden decline in kidney function (over hours to days) that inhibits the ability to regulate fluid, electrolyte and acid-base balance. Characterised by a reduction in the GFR (elevation of blood urea and plasma creatinine). Usually oliguria (urine output of less than 0.5 mL/kg/hr). Mostly reversible if diagnosed/treated early. Commonly results from extracellular volume depletion, decreased renal blood flow, or toxic/inflammatory injury. Can be classified as prerenal, intrarenal or postrenal (obstructive)

Question 25

AKD management

Answer 25

Prevention (by the maintenance of fluid volume before and after surgery or diuretics). Correcting physiological alterations (correct fluid and electrolyte disturbances, treat infections, maintain nutrition, precautionary measures). Renal replacement therapy in the form of haemodialysis may be indicated.

Question 26

Chronic kidney disease (CKD)

Answer 26

A complex disease caused by a variety of different pathophysiological conditions. Progressive loss of renal function over months or years by a complication of systemic diseases (hypertension or diabetes) and a complication of renal diseases (chronic glomerulonephritis, chronic pyelonephritis or chronic obstruction). Markers of kidney damage; urine protein, ultrasound, CT scan, X-ray (show small kidney size), renal biopsy for diagnosis confirmation

Question 27

CKD symptoms and clinical manifestations

Answer 27

Azotaemia (increased levels of serum urea and other nitrogenous compounds related to decreasing kidney function) and uraemic syndrome, aka uraemia (systemic symptoms associated with accumulation of nitrogenous wastes from protein metabolism and toxins in the plasma)

Question 28

CKD management

Answer 28

Dietary control (protein restriction, supplement vitamin D, fluid restriction). Erythropoietin replacement therapy, ACE inhibitors or receptor blockers, control of hyperglycaemia by insulin therapy, end-stage kidney disease leads to dialysis and kidney transplantation

Question 29

Prerenal AKI

Answer 29

Caused by impaired renal blood flow that causes cell injury. Can result from renal vasoconstriction, hypotension, hypovolaemia, haemorrhage

Question 30

Intrarenal AKI

Answer 30

Caused by acute tubular necrosis, nephrotoxins, sepsis, severe trauma including severe burns, acute glomerulonephritis, allograft rejection, interstitial disease

Question 31

Postrenal (obstructive) AKI

Answer 31

Caused by urinary tract obstruction (bladder outlet obstruction, prostatic hypertrophy, bilateral ureteral obstruction) or after catheterisation of the ureters (which may cause oedema)

Question 32

CKD effects on Neurological

Answer 32

Headache, drowsiness, sleep disorders, impaired concentration. Neuromuscular irritation causes hiccups, muscle cramps and twitching. End-stage kidney disease may progress to seizures and coma

Question 33

CKD effects on Integumentary

Answer 33

Uraemic skin residues (aka uraemic frost) cause inflammation, irritation and pruritus with scratching, excoriation and increased infection risk

Question 34

CKD effects on Fluid and electrolyte

Answer 34

Significant imbalance in CKD. Sodium and water retention cause oedema and hypertension. Potassium retention increasing to life-threatening levels

Question 35

CKD effect on Cardiovascular

Answer 35

Excess sodium and fluid volume leads to hypertension. Declining erythropoietin production leads to anaemia and increasing cardiac workload

Question 36

Diuretics

Answer 36

Diuretics are prescribed for treatment of hypertension, oedematous conditions, chronic renal failure and nephrotic syndrome. 3 main classes of diuretics are loop diuretics, thiazide diuretics and potassium-sparing diuretics

Question 37

Loop diuretics (e.g. furosemide)

Answer 37

In the thick ascending loop of Henle, they inhibit the Na+–K+–2 Cl– co-transporter (NKCC), thus preventing reabsorption of sodium and chloride. As this site accounts for about 15–25% of the reabsorption of sodium and chloride, their diuretic effect is greater than that the other diuretics (potent). Indication is often oedema associated with heart failure or severe hypercalcaemia.

Question 38

Thiazide diuretics (e.g. hydrochlorothiazide)

Answer 38

Act in the distal convoluted tubule where they inhibit reabsorption of sodium by blocking the Na+–Cl– symporter. The maximum portion of the sodium load they can affect at the distal tubule is ~5%, making them moderately potent diuretics in comparison with loop diuretics. Like the loop diuretics, they also increase potassium excretion. Indications include mild to moderate hypertension and oedema associated with heart failure or cirrhosis with ascites

Question 39

Potassium-sparing diuretics (e.g. spironolactone)

Answer 39

Limited diuretic efficacy, making them primarily useful when combined with potassium-depleting diuretics such as thiazides. Spironolactone blocks the action of aldosterone leading to the inhibition of the sodium-retaining property of aldosterone and a concomitant reduction in its potassium-secreting property. Indications include hypertension and oedema