remediation Flashcards

1
Q

Hashimoto’s Thyroiditis

A
  • Chronic autoimmune thyroiditis

- the most common cause of hypothyroidism in iodine sufficient areas

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2
Q

Clinical characterization of Hashimoto’s thyroiditis

A
  • Gradual thyroid failure, with or without goiter formation
  • High serum concentrations of antibodies against thyroid antigens
  • Follicular destruction
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3
Q

Cause of Hashimoto’s thyroiditis

A

combination of genetic susceptibility and environmental factors

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4
Q

Hashimoto’s : thyroid antigens

A

Thyroglobulin (Tg)
Thyroid Peroxidase (TPO)
TSH receptor

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5
Q

Hashimoto’s: Role of B cells

A
  • Nearly all patients with Hashimoto’s have high serum concentrations of antibodies to Tg and TPO
  • TSH receptor antibodies block the action of TSH
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6
Q

Hashimoto’s: Role of T cells

A
  • Apoptotic destruction of thyroid cells by activating cytotoxic T cells
  • Regulation of the local immune response
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7
Q

Pheochromocytoma

A
  • 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
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8
Q

Clinical Features of Pheochromocytoma

A

TRIAD: Headache, Palpitations, and Sweating

-life threatening acute hypertensive emergencies

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9
Q

Hormones affect on GFR

A

Norepinephrine: Decrease

Epinephrine: Increase

Endothelin: Decrease

Angiotensin II: neutral (prevents decrease)

Endothelial derived Nitric Oxide: Increase

Prostaglandins: Increase

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10
Q

Determinants of GFR

A
  • Glomerular/ Bowman’s Capsule: Hydrostatic Pressure

- Glomerular Capillary Colloid Osmotic: Oncotic Pressure

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11
Q

Earliest manifestation of Diabetic Nephropathy

A

Microalbuminuria

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12
Q

Albumin Excretion Rate

A

> 30 mg/day, <300 mg/day

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13
Q

Minimal Change Disease Microscopy

A

Light Microscopy: typically shows normal glomeruli

Electron Microscopy: shows diffuse effacement of the epithelial cell’s foot processes

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14
Q

Pathophysiological findings in Minimal Change Disease

A
  • 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
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15
Q

G6PD deficiency etiology

A

Decreased G6PD deficiency leads to Oxidative Injury leads to Hemolysis

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16
Q

G6PD pathogenesis

A
  • 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
17
Q

G6PD Causes

A
  • 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
18
Q

How many nephrons are in each kidney?

A

1 million

19
Q

How much blood flow does the kidney receive?

A

~22% CO
1100ml/min
~650 ml of plasma

20
Q

Different steps in Urine Formation

A

Glomerular Filtration, Tubular Reabsorption, Tubular Secretion

21
Q

Glomerular Filtration

A

Non selective; averages 20% of renal plasma flow

22
Q

Tubular Reabsorption

A

Highly variable and selective; most electrolytes and nutritional substances are almost completely reabsorbed

23
Q

Tubular Secretion

A

Highly variable; important for rapidly excreting some waste products, foreign substances and toxins

24
Q

Chronic Pyelonephritis

A

Chronic tubulointerstitial inflammation and scarring involve the calyces and pelvis

25
Q

Causes of Chronic Pyelonephritis

A
  • Chronic Kidney Disease
  • Chronic Obstructive Pyelonephritis (obstruction ->kidney infection -> scarring)
  • Reflux Nephropathy: from Superimposition of a UTI on congenital vesicoureteral reflux and intrarenal reflux
26
Q

Features of Chronic Pyelonephritis

A
  • Gradual Onset of renal insufficiency
  • HTN, asymmetrically contracted kidney
  • Bilateral disease (hyposthenuria manifested by polyuria and nocturia)
27
Q

Thalassemia Syndrome

A

Caused by inherited mutations that decrease the synthesis of either the alpha or beta globin chains that compose adult hemoglobin

28
Q

Mechanism for Thalassemia

A
  • 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
29
Q

When theres decrease hepcidin

A

iron overload due to excessive absorption of dietary iron

30
Q

Loop of Henle in countercurrent exchange system

A

serves as multipliers of the concentration gradient

31
Q

Vasa Recta in Countercurrent exchange system

A

a countercurrent exchanger for maintaining the gradient