remediation Flashcards
Hashimoto’s Thyroiditis
- Chronic autoimmune thyroiditis
- the most common cause of hypothyroidism in iodine sufficient areas
Clinical characterization of Hashimoto’s thyroiditis
- Gradual thyroid failure, with or without goiter formation
- High serum concentrations of antibodies against thyroid antigens
- Follicular destruction
Cause of Hashimoto’s thyroiditis
combination of genetic susceptibility and environmental factors
Hashimoto’s : thyroid antigens
Thyroglobulin (Tg)
Thyroid Peroxidase (TPO)
TSH receptor
Hashimoto’s: Role of B cells
- Nearly all patients with Hashimoto’s have high serum concentrations of antibodies to Tg and TPO
- TSH receptor antibodies block the action of TSH
Hashimoto’s: Role of T cells
- Apoptotic destruction of thyroid cells by activating cytotoxic T cells
- Regulation of the local immune response
Pheochromocytoma
- Catecholamine secreting tumors originating from chromaffin cells and the sympathetic ganglia are referred to as “pheochromocytomas” and “catecholamine secreting paragangliomas”
- The concentration of dopamine, norepinephrine, and epinephrine varies in every tumor
Clinical Features of Pheochromocytoma
TRIAD: Headache, Palpitations, and Sweating
-life threatening acute hypertensive emergencies
Hormones affect on GFR
Norepinephrine: Decrease
Epinephrine: Increase
Endothelin: Decrease
Angiotensin II: neutral (prevents decrease)
Endothelial derived Nitric Oxide: Increase
Prostaglandins: Increase
Determinants of GFR
- Glomerular/ Bowman’s Capsule: Hydrostatic Pressure
- Glomerular Capillary Colloid Osmotic: Oncotic Pressure
Earliest manifestation of Diabetic Nephropathy
Microalbuminuria
Albumin Excretion Rate
> 30 mg/day, <300 mg/day
Minimal Change Disease Microscopy
Light Microscopy: typically shows normal glomeruli
Electron Microscopy: shows diffuse effacement of the epithelial cell’s foot processes
Pathophysiological findings in Minimal Change Disease
- selective proteinuria, no HTN, preserved renal function
- Most frequent cause of nephrotic syndrome in kids
- Response to corticosteroids
- Primary: Idiopathic
- Secondary: Drugs, Neoplasms, Infections, Allergy
G6PD deficiency etiology
Decreased G6PD deficiency leads to Oxidative Injury leads to Hemolysis
G6PD pathogenesis
- Reduced Glutathione (GSH)- required to neutralize compounds such as H2O2
- X-Linked recessive (more males affected)
- 2-3 days after exposure -> hemolysis
- GSH -> oxidants “attack” of Hb -> Hb denatures and precipitates -> Heinz bodies -> intravascular hemolysis
- other cells with lesser damage -> extravascular hemolysis
G6PD Causes
- Infections (viral hepatitis, pneumonia)
- Drugs like antimalarials, sulfonamides, nitrofurantoin, phenacetin, aspirin
- Vitamin K foods (Fava beans)
- Oxidants that cause both IV and EV hemolysis in G6PD deficient individuals
How many nephrons are in each kidney?
1 million
How much blood flow does the kidney receive?
~22% CO
1100ml/min
~650 ml of plasma
Different steps in Urine Formation
Glomerular Filtration, Tubular Reabsorption, Tubular Secretion
Glomerular Filtration
Non selective; averages 20% of renal plasma flow
Tubular Reabsorption
Highly variable and selective; most electrolytes and nutritional substances are almost completely reabsorbed
Tubular Secretion
Highly variable; important for rapidly excreting some waste products, foreign substances and toxins
Chronic Pyelonephritis
Chronic tubulointerstitial inflammation and scarring involve the calyces and pelvis
Causes of Chronic Pyelonephritis
- Chronic Kidney Disease
- Chronic Obstructive Pyelonephritis (obstruction ->kidney infection -> scarring)
- Reflux Nephropathy: from Superimposition of a UTI on congenital vesicoureteral reflux and intrarenal reflux
Features of Chronic Pyelonephritis
- Gradual Onset of renal insufficiency
- HTN, asymmetrically contracted kidney
- Bilateral disease (hyposthenuria manifested by polyuria and nocturia)
Thalassemia Syndrome
Caused by inherited mutations that decrease the synthesis of either the alpha or beta globin chains that compose adult hemoglobin
Mechanism for Thalassemia
- Decrease HbA formation -> microcytic, hypochromic red cells
- Accumulation of unpaired alpha globin chains -> toxic precipitates that severely damage the membranes of red cells and erythroid precursors -> ineffective erythropoiesis
When theres decrease hepcidin
iron overload due to excessive absorption of dietary iron
Loop of Henle in countercurrent exchange system
serves as multipliers of the concentration gradient
Vasa Recta in Countercurrent exchange system
a countercurrent exchanger for maintaining the gradient
