Structure and Function - Cumulative Disorders (Final)

Diabetes Mellitus (Type 1 & 2) - Pathophysiology

Chronic hyperglycemia resulting from absolute insulin deficiency or peripheral resistance

Diabetes Mellitus (Type 1 & 2) - Urinary Link

When blood glucose exceeds the renal threshold, the excess glucose acts as an osmotic diuretic. This prevents water reabsorption, leading to polyuria and dehydration.

Diabetes Mellitus (Type 1 & 2) - Cardiovascular Link

Microvascular damage (nephropathy/retinopathy) and accelerated atherosclerosis.

Diabetes Insipidus - Pathophysiology

Deficiency of ADH (Central) or renal insensitivity to ADH (Nephrogenic).

Diabetes Insipidus - Urinary Link

Without ADH, aquaporins are not inserted into the collecting ducts. The kidneys cannot concentrate urine, leading to the excretion of high volumes of dilute urine with a very low specific gravity.

Diabetes Insipidus - Cardiovascular Link

Massive fluid loss leads to decreased blood volume and compensatory tachycardia to maintain cardiac output.

Hyperthyroidism (Grave's Disease) - Pathophysiology

Excessive production of T3/T4, dramatically increasing the Basal Metabolic Rate.

Hyperthyroidism (Grave's Disease) - Cardiovascular Link

Thyroid hormones upregulate beta-adrenergic receptors in the heart, leading to increased heart rate, palpitations, and potentially atrial fibrillation.

Hyperthyroidism (Grave's Disease) - Digestive Link

Stimulates hypermotility of the GI tract, resulting in hyperdefecation and malabsorption.

Addison's Disease - Pathophysiology

Primary adrenal insufficiency causing a deficiency in mineralocorticoids (aldosterone) and glucocorticoids (cortisol).

Addison's Disease - Urinary Link

Lack of aldosterone prevents sodium reabsorption and potassium secretion. This leads to hyponatremia and life-threatening hyperkalemia. Don't forget about lower glucose here too!

Addison's Disease - Cardiovascular Link

The loss of sodium and water results in chronic hypotension and decreased cardiac output.

Cushing Syndrome - Pathophysiology

Chronic hypercortisolism, often from an adrenal tumor or prolonged steroid use.

Cushing Syndrome - Digestive Link

Cortisol increases gastric acid secretion while thinning the mucosal barrier, heightening the risk of peptic ulcers.

Cushing Syndrome - Urinary Link

Excess cortisol cross-reacts with mineralocorticoid receptors, leading to sodium retention, edema, and hypertension. Of course, glucose is high here. I wonder which other diseases on this list, we could jump to from here...

Hemochromatosis - Pathophysiology

Genetic disorder causing excessive iron absorption and deposition in tissues (hemosiderosis).

Hemochromatosis - Digestive Link

Iron deposition in the liver causes oxidative stress, leading to cirrhosis and hepatomegaly, and decreased liver function.

Hemochromatosis - Other Links

Deposition in the pancreatic beta cells causes cell death, leading to "bronze diabetes." Depositions in the skin and liver cirrhosis → jaundice contribute to this color.

Pernicious Anemia - Pathophysiology

Autoimmune destruction of parietal cells in the stomach lining.

Pernicious Anemia - Digestive Link

Loss of parietal cells leads to a lack of Intrinsic Factor.

Pernicious Anemia - Blood Link

Vitamin B12 cannot be absorbed without Intrinsic Factor, resulting in macrocytic anemia (abnormally large RBCs; don't carry oxygen efficiently). How does the cardiovascular system react to this? And, what would the kidney do to compensate?

CV: compensates by pumping more (↑ HR + ↑ SV) → maintain oxygen delivery

Kidney: compensates by releasing EPO → try to increase RBC production

Disseminated Intravascular Coagulation (DIC) - Pathophysiology

Systemic activation of the coagulation cascade, often secondary to sepsis.

Disseminated Intravascular Coagulation (DIC) - Blood Link

Widespread clotting depletes the supply of platelets and clotting factors, leading to simultaneous systemic clotting and uncontrollable bleeding.

Disseminated Intravascular Coagulation (DIC) - Cardiovascular Link

Micro-clots lead to tissue ischemia and multi-organ failure. Bleeding internally also isn't a good thing.

Right-Sided Heart Failure (RHF) - Pathophysiology

Inability of the right ventricle to pump blood into the pulmonary circuit.

Right-Sided Heart Failure (RHF) - Digestive Link

Backflow into the IVC and hepatic veins causes congestive hepatomegaly (enlarged liver) and ascites (abdominal fluid buildup).

Right-Sided Heart Failure (RHF) - Lymphatic Link

Increased systemic venous pressure prevents lymph drainage, causing peripheral pitting edema.

Left-Sided Heart Failure (LHF) - Pathophysiology

Failure of the left ventricle to maintain systemic cardiac output.

Left-Sided Heart Failure (LHF) - Respiratory Link

Backflow into the pulmonary veins increases hydrostatic pressure in pulmonary capillaries, forcing fluid into the alveoli (Pulmonary Edema).

Left-Sided Heart Failure (LHF) - Urinary Link

Decreased renal perfusion triggers the RAAS pathway, causing salt and water retention.

Hypovolemic Shock - Pathophysiology

Loss of >20% of blood or interstitial fluid volume.

Hypovolemic Shock - Cardiovascular Link

Decreased venous return leads to a drop in stroke volume and MAP.

Hypovolemic Shock - Urinary Link

Blood is shunted away from the kidneys to preserve core pressure, leading to oliguria or anuria.

Cardiac Tamponade - Pathophysiology

Fluid accumulation in the pericardial sac that compresses the heart.

Cardiac Tamponade - Cardiovascular Link

External pressure prevents the ventricles from expanding during diastole, causing a drop in preload and stroke volume.

Cardiac Tamponade - Urinary Link

Triggers a heavy RAAS response due to the drop in systemic blood pressure.

Portal Hypertension - Pathophysiology

Increased resistance to blood flow through the liver (often due to cirrhosis).

Portal Hypertension - Digestive Link

Blood pushed into nearby vessels, leading to esophageal varices (enlarged veins in lower esophagus (only part drained (eventually) by the portal venous system). These are not designed for high volume or pressure!

Portal Hypertension - Blood Link

Pressure backs up into the splenic vein, causing splenomegaly (spleen enlargement) and the destruction of RBCs and platelets.

Superior Vena Cava (SVC) Syndrome - Pathophysiology

Obstruction of the SVC; example: mediastinal tumor

Superior Vena Cava (SVC) Syndrome - Cardiovascular/Lymphatic Link

Blocked drainage from the head/neck leads to facial edema and distended neck veins. Not just because they're angry and yelling in this case.

Superior Vena Cava (SVC) Syndrome - Respiratory Link

Can cause laryngeal edema, leading to dyspnea (shortness of breath) and/or stridor (high pitched breathing sounds due to airway obstruction.

Respiratory Acidosis - Pathophysiology

Hypoventilation leading to CO2 retention.

Respiratory Acidosis - Respiratory Link

Common in COPD (See SVC respiratory link above) or drug-induced respiratory depression

Respiratory Acidosis - Urinary Link

The kidneys compensate by secreting H+ and reabsorbing HCO3- to raise blood pH.

· Do not give this person the bag.

Respiratory Alkalosis - Pathophysiology

Hyperventilation leading to excessive loss of CO2.

Respiratory Alkalosis - Respiratory Link

Triggered by high altitude (Why might this occur? - bc of low O2 levels so trying to breathe more), anxiety, or pulmonary embolism.

Respiratory Alkalosis - Urinary Link

The kidneys compensate by excreting HCO3- into the urine to lower blood pH. This unmasks the H+.

· Give this person the bag.

Metabolic Acidosis - Pathophysiology

Accumulation of acids or loss of bicarbonate (diarrhea).

Metabolic Acidosis - Endocrine/Urinary Link

Seen in Diabetic Ketoacidosis (DKA) (glucose is back...again) or Renal Failure (decreased excretion of H+). You could probably (definitely) link a hormone to this - Aldosterone

Metabolic Acidosis - Respiratory Link

The lungs compensate via Kussmaul breathing (deep, rapid hyperventilation) to blow off CO2 and raise pH. Lungs Save the day!

Metabolic Alkalosis - Pathophysiology

Excess bicarbonate intake (overuse of antacids) or loss of acid (21st birthday?)

Metabolic Alkalosis - Digestive Link

Commonly caused by severe vomiting loss of HCl

Metabolic Alkalosis - Respiratory Link

The lungs compensate by hypoventilating (slowing the rate) to retain CO2 and lower pH

Tension Pneumothorax - Pathophysiology

Air enters the pleural space but cannot escape, building positive pressure.

Tension Pneumothorax - Respiratory Link

Complete collapse of the lung on the affected side. Tracheal deviation contralaterally

Tension Pneumothorax - Cardiovascular Link

Mediastinal shift compresses the Vena Cava, leading to a sudden drop in venous return and obstructive shock

- This person needs emergency treatment. Atelectasis (lung collapse) isn't emergent.

Chronic Bronchitis - Pathophysiology

Hypertrophy of mucus glands and chronic airway inflammation.

Chronic Bronchitis - Respiratory Link

Airway obstruction leads to persistent hypoxemia. Check back in with some other respiratory diseases above.

Chronic Bronchitis - Blood Link

Chronic hypoxia triggers the kidneys to release Erythropoietin (EPO), causing secondary polycythemia (↑ red blood cells (RBCs) → ↑ hemoglobin → ↑ oxygen-carrying capacity)