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Questions and Answers

What is the primary factor that contributes to reduced glomerular filtration rate (GFR) in nephritic syndrome?

  • Increased tubular reabsorption of water
  • Elevated hydrostatic pressure in capillaries
  • Increased renal blood flow
  • Decreased glomerular membrane permeability (correct)

Which physiological change is associated with secondary hyperparathyroidism in chronic kidney disease?

  • Decreased inactivation of insulin-like growth factor-1 (IGF-1) (correct)
  • Decreased levels of vasopressin
  • Increased inactivation of parathyroid hormone (PTH)
  • Increased clearance of water and solutes

What causes the skin hyperpigmentation seen in primary hypocorticism?

  • Decreased levels of Melanocyte Stimulating Hormone (MSH)
  • Elevated levels of cortisol
  • Increased synthesis of Proopiomelanocortin (POMC) (correct)
  • Enhanced secretion of ACTH

Which metabolic products accumulate in liver failure leading to metabolic acidosis?

<p>β-hydroxybutyric acid and acetoacetic acid (C)</p> Signup and view all the answers

What is a key characteristic of the renin-angiotensin-aldosterone system (RAAS) activation in nephritic renal edema?

<p>Sodium retention (D)</p> Signup and view all the answers

What metabolic condition is characterized by a rise in CO2 levels due to impaired clearance?

<p>Respiratory acidosis (C)</p> Signup and view all the answers

Which consequence is primarily associated with the reduced tubular water resorption in patients with decreased GFR?

<p>Hypervolemia (B)</p> Signup and view all the answers

Which condition is a potential outcome of decreased inactivation of erythropoietin in chronic kidney disease?

<p>Anemia (A)</p> Signup and view all the answers

What stool changes are commonly observed in patients with posthepatic jaundice?

<p>Stool is acholic and fatty in appearance (A)</p> Signup and view all the answers

Which of the following is a potential consequence of vitamin D deficiency in liver failure?

<p>Bone and muscle weakness (A)</p> Signup and view all the answers

What is a likely clinical manifestation of vitamin A deficiency in liver failure?

<p>Xerophthalmia and nightblindness (A)</p> Signup and view all the answers

What condition is associated with disaccharide maldigestion?

<p>Intestinal distension and flatulence (C)</p> Signup and view all the answers

Which electrolyte disturbance is linked with secondary hyperaldosteronism in liver failure?

<p>Hypernatremia due to sodium retention (C)</p> Signup and view all the answers

What laboratory finding is most likely in a patient with hypokalemia due to secondary hyperaldosteronism?

<p>Decreased potassium levels (D)</p> Signup and view all the answers

Which of the following symptoms is NOT typically associated with liposoluble vitamin D deficiency in liver failure?

<p>Enhanced muscle strength (C)</p> Signup and view all the answers

What effect does disaccharide maldigestion have on hydration status?

<p>Hypovolemia from osmotic diarrhea (D)</p> Signup and view all the answers

What is a consequence of hypochlorhydria on gastric tone and motility?

<p>hypotonia (B)</p> Signup and view all the answers

Which type of maldigestion occurs due to pancreatic exocrine deficiency?

<p>protein maldigestion (C)</p> Signup and view all the answers

How is carbohydrate metabolism in hepatocytes affected during liver failure?

<p>reduced glucose level in fasting (B)</p> Signup and view all the answers

What change occurs in the concentration of branched amino acids in liver failure?

<p>Increased due to their increased breakdown in peripheral tissue (D)</p> Signup and view all the answers

What type of metabolic change is triggered in type I diabetes mellitus?

<p>metabolic acidosis caused by accumulation of acetylacetic acid (A)</p> Signup and view all the answers

In primary hypothyroidism, what is the expected blood hormone concentration?

<p>low thyroid-releasing hormone, high thyrotropin, decreased thyroid hormones (A)</p> Signup and view all the answers

What change occurs in blood hormone concentration in secondary hypothyroidism?

<p>increased thyroid-releasing hormone, increased thyrotropin, low thyroid hormones (A)</p> Signup and view all the answers

How does tertiary hyperthyroidism affect blood hormone concentrations?

<p>increased thyroid-releasing hormone, low thyrotropin, raised thyroid hormones (A)</p> Signup and view all the answers

What condition is characterized by increased hydrogen ion excretion and an alkaline state in the blood?

<p>Metabolic alkalosis (D)</p> Signup and view all the answers

Which of the following is NOT associated with secondary hyperaldosteronism?

<p>Metabolic acidosis (B)</p> Signup and view all the answers

Which of the following is a production function of the kidneys?

<p>Production of calcitriol (D)</p> Signup and view all the answers

Which feature is NOT characteristic of hepatocyte apoptosis?

<p>Cell swelling (D)</p> Signup and view all the answers

What process leads to the release of cellular contents due to defective osmotic regulation in hepatocyte necrosis?

<p>Rupture of the cell (C)</p> Signup and view all the answers

In hepatocyte apoptosis, what term describes the condensation of nuclear chromatin?

<p>Pyknosis (B)</p> Signup and view all the answers

What type of necrosis is characterized by widespread loss of hepatocytes, often seen in acute toxic injuries?

<p>Confluent necrosis (A)</p> Signup and view all the answers

What term describes the smaller, acidophilic fragments that result from hepatocyte fragmentation during apoptosis?

<p>Apoptotic bodies (A)</p> Signup and view all the answers

What condition leads to hypocalcemia and secondary hyperparathyroidism?

<p>Impaired Vitamin D Synthesis (C)</p> Signup and view all the answers

What skin condition is characterized by the deposition of crystallized urea?

<p>Uremic Frost (D)</p> Signup and view all the answers

What causes osteodystrophy in patients with kidney dysfunction?

<p>Altered calcium-phosphate metabolism (D)</p> Signup and view all the answers

What is the result of impaired response to infections in patients with renal failure?

<p>Immune Dysfunction (D)</p> Signup and view all the answers

What effect does high urea levels have on proteins?

<p>Protein Destabilization (C)</p> Signup and view all the answers

What is the primary hematological change associated with hypersplenism in liver failure?

<p>Anemia due to reduced red blood cell lifespan (A)</p> Signup and view all the answers

Which neurological complication can occur during chronic renal failure?

<p>Uremic Encephalopathy leading to confusion (B)</p> Signup and view all the answers

Which of the following gastrointestinal manifestations is NOT typically associated with chronic renal failure?

<p>Bloating and gas (A)</p> Signup and view all the answers

What is a cardiovascular disorder resulting from chronic renal failure?

<p>Hypertension due to fluid retention (A)</p> Signup and view all the answers

What causes the anemia observed in patients with chronic renal failure?

<p>Decreased erythropoietin production (B)</p> Signup and view all the answers

Which complication is linked with accelerated atherosclerosis in chronic renal failure?

<p>Dyslipidemia (A)</p> Signup and view all the answers

What is a potential immune system disorder related to renal failure?

<p>Increased susceptibility to infections (C)</p> Signup and view all the answers

Which of the following indicates a fluid and electrolyte imbalance in chronic renal failure?

<p>Hyperkalemia (D)</p> Signup and view all the answers

Flashcards

Reduced GFR in nephritic syndrome

Decreased glomerular membrane permeability leads to decreased GFR, causing fluid retention and buildup of waste products.

Nephritic renal edema pathogenesis

Increased glomerular capillary wall permeability, sodium retention, and activation of the RAAS (renin-angiotensin-aldosterone system) lead to water and solute retention.

Hormone inactivation in CKD

Impaired kidney function causes reduced inactivation of hormones like PTH, IGF-1, and vasopressin, leading to secondary issues like hyperparathyroidism, growth problems, and fluid imbalances.

Secondary hyperparathyroidism

Reduced inactivation of parathyroid hormone (PTH) in the kidneys leads to increased PTH levels, leading to bone disease and soft tissue calcification.

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Metabolic acidosis in liver failure

Liver failure leads to the accumulation of acidic products like beta-hydroxybutyric acid and acetoacetic acid, causing metabolic acidosis.

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Primary hyperaldosteronism cause

Usually caused by a hormone-secreting tumor in the adrenal gland that produces excessive aldosterone.

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Primary hypocorticism skin pigmentation

Reduced cortisol feedback leads to increased ACTH and MSH, causing skin hyperpigmentation.

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Hyperchlorhydria stomach effects

In hyperchlorhydria (high stomach acid), the stomach may experience unusual tone or motility (e.g. hypertonus, trouble emptying).

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Hypochlorhydria Stomach Issues

Hypochlorhydria, a condition with low stomach acid, leads to decreased gastric tone (hypotonia) and slowed stomach motility.

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Pancreatic Exocrine Deficiency Digestion

Pancreatic exocrine deficiency impairs digestion of carbohydrates, proteins, and lipids, leading to maldigestion.

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Liver Failure and Carbohydrate Metabolism

In liver failure, carbohydrate metabolism is disrupted, typically leading to reduced glucose levels during fasting and reduced glycogen storage.

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Liver Failure and Amino Acid Levels

Liver failure changes amino acid levels in the blood, increasing branched-chain amino acids due to increased breakdown in tissues, and increasing aromatic amino acids due to reduced breakdown by the liver.

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Type 1 Diabetes and Acid-Base

Type 1 diabetes can cause metabolic acidosis due to the accumulation of acidic substances like acetoacetic acid (and potentially others like oxaloacetate).

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Primary Hypothyroidism Hormone Changes

Primary hypothyroidism results in low thyroid hormones, low TSH, and low TRH (Thyroid-releasing hormone, which usually stimulates TSH).

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Secondary Hypothyroidism Hormone Changes

Secondary hypothyroidism results in low thyroid hormones, low TSH, and low TRH.

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Tertiary Hyperthyroidism Hormone Changes

Tertiary hyperthyroidism has increased TRH, low TSH, and high thyroid hormone.

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Uremic Frost

Crystallized urea deposits on the skin, seen in severe kidney failure.

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Oliguria

Reduced urine output, often less than 400 ml/day, a sign of kidney dysfunction.

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What causes Pruritus in kidney failure?

Pruritus, or severe itching, in kidney failure is caused by uremic toxins and secondary hyperparathyroidism.

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How does Oxidative Stress damage in kidney failure?

Uremic toxins like dimethyl-arginine, methylglyoxal, and phenols cause systemic damage, leading to increased blood pressure, cell lysis, and protein destabilization.

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What is Renal Osteodystrophy?

Bone disease in kidney failure due to altered calcium-phosphate metabolism and vitamin D deficiency.

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Posthepatic jaundice stool changes

Feces lack bile (acholia), are discolored, and appear fatty (steatorrhea).

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Liver failure vitamin D deficiency symptoms

Bone and muscle weakness (osteoporosis), hypokalaemia, impaired immune system, mood changes (depression, anxiety), increased risk of chronic disorders (cardiovascular disease, diabetes, cancer) and impaired wound healing.

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Liver failure vitamin A deficiency symptoms

Impaired vision (keratinomalacia), xerophthalmia, night blindness, epithelium changes, immune deficiency, hyperplasia, hyperkeratinization, and urinary stones/cell metaplasia of the gastrointestinal, urinary, and respiratory tracts.

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Disaccharide maldigestion consequences

Intestinal distension, flatulence, isotonic dehydration, osmotic diarrhea, dehydration (hypovolemia), and hypoglycemia. May also include pancreatic insufficiency.

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Secondary hyperaldosteronism electrolytic disturbance

Hypernatremia (high sodium) and hypokalemia (low potassium).

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Hypernatremia cause

Excessive sodium retention, due to high aldosterone levels, resulting in elevated sodium levels in the bloodstream.

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Hypokalemia cause

Increased potassium excretion , leading to low potassium levels in the blood.

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Hypernatremia effect

Intracellular hyperosmolarity, water shift into cells; cellular swelling(incl. edema in cells, endothelia), causing narrowing of vascular lumen

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Hypersplenism in Liver Failure

A condition where the enlarged spleen in liver failure traps and destroys blood cells leading to low counts of red blood cells (anemia), platelets (thrombocytopenia), and white blood cells (leukopenia).

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Uremic Encephalopathy

A neurological complication of chronic kidney failure caused by the accumulation of toxins in the blood, leading to brain dysfunction manifested as confusion, lethargy, seizures, or coma.

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Peripheral Neuropathy in CKD

A neurological complication of chronic kidney failure affecting the peripheral nerves, causing tingling, numbness, and weakness in the extremities.

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Hypertension in CKD

High blood pressure in chronic kidney failure is caused by fluid retention and activation of the renin-angiotensin-aldosterone system, which helps regulate blood pressure.

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Left Ventricular Hypertrophy (LVH) in CKD

LVH in chronic kidney failure is caused by chronic hypertension and volume overload, putting extra strain on the heart's left ventricle.

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Anemia in CKD

Anemia in chronic kidney failure occurs due to reduced erythropoietin production (hormone that stimulates red blood cell production) by the kidneys, and hemolysis caused by uremic toxins.

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Uremic Fetor

An ammonia-like odor on the breath caused by the breakdown of urea in saliva, occurring as a result of chronic kidney failure.

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Increased Susceptibility to Infections in CKD

Chronic kidney failure weakens the immune system due to uremic toxins and malnutrition, increasing the risk of getting infections.

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Metabolic Alkalosis

A condition where the blood becomes alkaline due to an increase in hydrogen ion excretion.

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Secondary Hyperaldosteronism in Metabolic Alkalosis

A condition where excessive aldosterone production leads to decreased urine output, lower urine osmolarity, and a less acidic urine pH, contributing to metabolic alkalosis.

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Kidney Endocrine function: Local Activation of the Kallikrein system

This function refers to the kidneys' ability to activate the kallikrein system locally, involving enzymes that help regulate blood pressure and fluid balance.

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Kidney Endocrine function: Paracrine Secretion of Vasodilator Prostaglandins

The kidneys secrete prostaglandins that act locally to dilate blood vessels, helping regulate blood flow and blood pressure.

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Kidney Endocrine function: Calcitriol Production

The kidneys produce calcitriol, the active form of vitamin D, which is crucial for calcium absorption and maintaining bone health.

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Hepatocyte Apoptosis

A programmed cell death in the liver where affected hepatocytes shrink, their nuclei condense, fragment, and eventually break into apoptotic bodies.

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Hepatocyte Necrosis

An uncontrolled cell death in the liver where affected hepatocytes swell, rupture, and release their contents, causing inflammation and tissue damage.

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Councilman Bodies

Apoptotic hepatocytes that are characteristically found in yellow fever, reflecting the viral damage to the liver.

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Study Notes

Pathophysiology Questions

  • Acute Renal Failure (ARF) - Humoral Syndrome Manifestations:
    • Hyperazotemia
    • Oliguria (Low urine output)
    • Hypokalemia (low potassium)
    • Hyponatremia caused by hemodilution
  • Diuresis Changes in Hyperglycemia:
    • Osmotic diuresis caused by excess glucose in the urine increases urine production.
    • Kidney function can be impaired with damage to the glomeruli by hyperglycemia
    • Hormonal changes such as alteration in vasopressin production can affect sodium and water balance and urine output
  • Obstruction of Urinary Pathways:
    • Increased pressure leads to impaired filtration and backflow of urine
    • Hormonal changes are also a factor
  • Chronic Renal Failure (CRF) Manifestations:
    • Osteodystrophy
    • Iron deficiency anemia
    • Secondary hyperparathyroidism
    • Osteoporosis
  • Acute Renal Failure (ARF) Prerenal Causes:
    • Systemic vasodilation in spinal shock
    • Heart failure
    • High levels of catecholamines in the blood

Additional Pathophysiology Questions

  • Reduced Glomerular Filtration Rate (GFR) Consequences:
    • Fluid and Electrolyte imbalances
    • Waste product accumulation
    • Hypertension (high blood pressure)
    • Anemia (low red blood cells)
    • Bone disease
    • Cardiovascular disease.
  • Urinary Pathway Obstruction Consequences:
    • Hydronephrosis
    • Renal failure
    • Urinary tract infections
    • Stone formation
    • Pain and discomfort
    • Urinary incontinence.
  • Glomerulopathy with Nephritic Syndrome:
    • Increased blood pressure is caused by activity of RAAS, increased extracellular fluid, defects in endothelial function and inflammation
    • Genetic factors also play a role.
  • Nephrotic Syndrome Coagulopathy:
    • Loss of anticoagulant proteins
    • Increased levels of procoagulants
    • Endothelial dysfunction, and hyperlipidemia
  • Hypovolemia effect on GFR:
    • Reduced effective filtration pressure
    • Diminished hydrostatic pressure in glomerular capillaries
  • Nephritic Renal Edema:
    • Increased permeability in glomerular capillary wall
    • Sodium retention
    • Activation of Renin-Angiotensin-Aldosterone System (RAAS)
    • Decreased clearance of water and solutes
  • Hormone Inactivation in Kidney Disease:
    • Consequences of disturbances in hormone inactivation in the kidney are not explicitly described

Additional Pathophysiology Questions (Page 3)

  • Tertiary Hyperthyroidism Pathogenesis:
    • Increased TRH
  • Primary Hyperaldosteronism Cause:
    • Hormone-secreting tumor from the glomerular layer of the adrenal gland (usually an adenoma) or primary adrenocortical hyperplasia

Additional Pathophysiology Questions (Page 4)

  • Reduced Glomerular Filtration Rate (GFR) in Nephritic Syndrome:

    • Decreased glomerular membrane permeability
    • Fluid retention and accumulation of nitrogenous waste

  • Primary Hypocorticism:

    • Skin hyperpigmentation
    • Diminished cortisol negative feedback results in massive rise of MSH/ACTH which causes brown discoloration of the skin

  • Metabolic Acidosis in Liver Failure: Accumulation of certain metabolic products explains metabolic acidosis in liver failure (same answer as question 18)

  • β-hydroxybutyric acid

  • acetoacetic acid

Additional Pathophysiology Questions (Page 5-7 and further)

  • Hyperchlorhydria:
    • Gastric hypotonus
    • Accelerated evacuation
  • Hypochlorhydria:
    • Gastric hypertonicity
    • Slowed evacuation
  • Pancreatic Exocrine Deficiency:
    • Digestion of polysaccharides, proteins, or lipids is impaired
  • Hepatocyte Liver Failure:
    • Glucose levels increase after meals and decrease in fasting
    • Fructosemia
    • Reduced glycogen storage

Additional Pathophysiology Questions (Page 8 and further)

  • GH Hypersecretion:
    • Hyperglycemia
    • Enhanced glycogenolysis
    • Enhanced gluconeogenesis (from free fatty acids and glycerol)
  • Hypothyroidism:
    • Decreased basal metabolism
    • Oxidative phosphorylation disruption
    • Reduced oxidation processes
  • Hypervolemia Effects on GFR:
    • Reduced GFR
  • Hypothyroidism Lipid Metabolism:
    • Reduced lipolysis
    • Elevated cholesterol
  • Diabetes Mellitus Type I:
    • Increased lipolysis with enhanced oxidation of glycerol or FFA
  • Protein Metabolism:
    • Increased protein breakdown = negative nitrogen balance (often related to insulin def.)
  • Type I Diabetes Mellitus Protein Metabolism:
    • Reduced lypolysis and proteolysis due to insulin lack
    • Enhanced proteolysis and lypolisis from catecholamine deficiency
    • Enhanced proteolysis and lypolisis due to glucocortocosteroid deficiency
  • Hemorrhagic Syndrome in Hepatic/Posthepatic Jaundice:
    • Due to increased concentration of biliary acids (cholalemia).

Additional Pathophysiology Questions (Page 10-11)

  • Hyperaldosteronism Manifestations:
    • Increased resistance in peripheral blood vessels
    • Urine hyperosmolarity
    • Excratory alkalosis

Additional Pathophysiology Questions (Page 12-13 and Further)

  • Kidney Injury:
    • Increased activity of ROS, cytokines, chemokines, and growth factors
  • Primary Hyperaldosteronism:
    • Problems with the hypothalamic-pituitary-adrenal (HPA) axis and or lack of negative feedback due to tumor in the pituitary will cause hypersecretion.

Additional Pathophysiology Questions (Page 14-15 and Further)

  • Disaccharide Maldigestion:
    • Intestinal distension and flatulence
    • Isotonic dehydration
    • Osmotic diarrhea

Additional Pathophysiology Questions (Page 16-17, and further)

  • Chronic Renal Failure Manifestations:
    • Fluid and electrolyte imbalances
    • Edema
    • Hyperkalemia
    • Hyponatremia
    • Metabolic acidosis
  • Uremic Encephalopathy:
    • Confusion, lethargy, and coma.
  • Peripheral Neuropathy:
    • Tingling, numbness, and motor weakness
  • Cardiovascular Disorders:
    • Hypertension (high blood pressure)
    • Left ventricular hypertrophy
    • Heart failure
    • Accelerated atherosclerosis (thickening of blood vessels)
    • Pericarditis

Additional Pathophysiology Questions (Page 18-19, and further)

  • Alcohol Toxicity:
    • Increased accumulation of triglycerides
    • Reduced fatty acid oxidation
    • Generation of reactive oxygen species and inflammation.
  • Glucocorticoids' Effect:
    • Increased lipolysis
    • Enhanced gluconeogenesis

Additional Questions (Page 20-22 and further)

  • Liver Failure pH Imbalance:
    • Reduced urea production causes hyperammonemia (pH<7.35)
    • Reduced gluconeogenesis from ketone bodies and lactic acid decrease the pH (pH <7.35)

Additional Questions (Page 23 and further)

  • Jaundice
    • Increased billirubin
    • Impaired bile flow to intestines causes jaundice
    • Conjugated or unconjugated types of billirubin differ in solubility, toxicity, and exit routes from the body

Additional Questions (Page 24 and further)

  • Unconjugated Hyperbilirubinemia:
    • Excessive production of bilirubin
    • Reduced uptake by the liver
    • Impaired bilirubin conjugation

Additional Questions (Page 25 and further)

  • Portal Hypertension
    • Increased resistance to flow in the portal venous system
    • Portal vein obstruction
    • Intrahepatic causes: alcoholic cirrhosis, schistosomiasis or fatty tissue
    • Post hepatic causes: obstruction of hepatic or venous outflow

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