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8 PATH 2 > LECTURE 2 > Flashcards

LECTURE 2 Flashcards

1
Q

IgA Nephropathy aka

A

Berger’s Disease

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2
Q

What is the MC disease worldwide?

A

IgA Nephropathy (aka Berger’s Disease)

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3
Q

What is the Most common cause of gross hematuria (brown urine)?

A

IgA Nephropathy. (Aka Berger’s Disease)

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4
Q

When does IgA nephropathy aka Berger’s Disease develop?

A

Within 1-2 days of an acute upper respiratory infection (common cold) OR

Acute gastrointestinal/urinary infection

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5
Q

Urination lasts for a while and then _______ in IgA Nephropathy (Berger’s)

A

Stops spontaneously

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6
Q

What is IgA nephropathy (Berger’s) characterized by?

A

By development of loin pain (low back/butt)

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7
Q

What is Increased in IgA Nephropathy/ Berger’s?

A

Increased concentration of IgA immunoglobulin in the blood circulation as well as increased concentration of IgA

Deposition of IgA complexes into mesangium** QUIZ

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8
Q

What is the role of IgA, and w

A

Protects mucus membranes during infection

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9
Q

What type of rash is seen with IgA nephropathy / Berger’s?

A

Henoch-Schonlein Purpura ** QUIZ

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10
Q

What is the prognosis of IgA Nephropathy aka Berger’s?

A

Different/varietal 10-20% will have kidney pathology -> kidney failure

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11
Q

Buerger’s disease aka

A

Thromboangiitis Obliterans

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12
Q

What is Buerger’s / Thromboangiitis Obliterans characterized by?

A

Acute/Chronic thrombizing inflammation of the middle small arteries (VASCULITIS)

ALSO with inflammation of VEINS (PHLEBITIS) and NERVES (vasonevorum)

1 arteries
2 veins
3 nerves

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13
Q

What is the biggest distinguishing factor about Buerger’s Disease aka Thromboangiitis Obliterans?

A

Only disease in the cardiovascular system with VASCULITIS involving arteries and veins **

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14
Q

Is Buerger’s associated with kidney pathology?

A

NO, it is a CARDIOVASCULAR system disease

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15
Q

What is Buerger’s Disease associated with?

A

Young < 35 yo smoking people, typically in younger females with heavy tobacco use

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16
Q

What does smoking do in Buerger’s disease?

A

Initiates and maintains the disease (quit smoking and the disease goes away)

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17
Q

What are the 3 manifestations of Buerger’s Disease?

A

1) . Instep Claudication
2) . Raynauds Phenomenon
3) . Thrombophlebitis

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18
Q

What is Instep Claudication?

A

Periodic spasm of artery associated with exertion

  • Patient experiences severe pain in the calf due to ischemia or neuropathy -> as you use the muscle, blood supply is needed, increased use cannot be supplied with enough blood/oxygen
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19
Q

What is Raynaud’s Phenomenon?

A

Vascular disease of the fingers -> Vasospastic reaction resulting in arteries, veins (WHITE, BLUE, RED)

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20
Q

What is Thrombophelbitis?

A

Inflammation of veins -> Formation of thrombytes -> can kill patient

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21
Q

If a patient continues to smoke with Buerger’s disease what will eventually happen?

A

They will develop gangrene due to narrowing of the arteries (usually vertebral, radial, and ulnar arteries)

  • Amputation is common
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22
Q

What is the best definition of Buerger’s Disease?

A

Nonarterosclerotic , segmental, inflammatory disease affecting small and medium sized arteries and veins of upper and lower extremities

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23
Q

Where does Buerger’s Disease occur?

A

Japan, Israel, and India

  • Predisposing factors are still unknown
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24
Q

Hereditary Glomerulonephritis aka

A

Alport Syndrome

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25
Q

What is Hereditary GMN aka Alport Syndrome?

A

Abnormal production of type 4 collagen (poor quality collagen/not stable)

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26
Q

Hereditary GMN (Alport) develops _____

A

In boy with impairment of type 4 collagen production (collagen in glands in basement membrane of capillaries; and early childhood (5-20 yo) first decade of life

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27
Q

What are the symptoms of Hereditary GMN aka Alport Syndrome?

A
  • Nerve deafness
  • Lens dislocation (lens made of collagen type 4)
  • Posterior cataracts
  • Corneal dystrophy (deaf and blind)
  • Usually become chronic and develop renal failure (20-25 yo) death by 20 yo
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28
Q

What is Nephrotic Syndrome clinically manifested by?

A

Dramatically increased permeability of proteins (albumin molecular cites) in glomeruli

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29
Q

How does the damage happen in Nephrotic Syndrome?

A

Damage to the cell membrane allowing proteins through, NOT water (due to the protein leaving, it takes water with it)

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30
Q

What are the 4 main symptoms of Nephrotic Syndrome?

A

1) . Massive (heavy) proteinuria (>3.5g/24hr)
2) . Hypoalbuminemia (<3.0 g/dL)
3) . Generalized edema
4) . Hyperlipidemia and lipiduria

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31
Q

In Nephrotic syndrome, what is Massive (heavy) proteinuria characterized by?

A

Proteins in the urine, there is a huge loss of proteins during filtration of blood in the kidney

  • Presence of protein in the urine indicates a decrease of albumin from the circulation
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32
Q

What is Hypoalbuminemia characterized by?

A

Inversion of albumin to globulin ratio (<1) leaving less proteins in the body

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33
Q

What is “Electrophoresis” associated with?

A

Hypoalbuminemia in Nephrotic Syndrome

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34
Q

What is Electrophoresis?

A

Albumin peak normally much higher than all others, peak decreases in size blood circulation, contains proteins

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35
Q

What is the normal protein ratio in the blood?

A

Albumin 55%
Globulin 40-45%
Fibrinogen 5-7%

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36
Q

What is the ratio that makes “Hypoalbuminemia?”

A

Normal - Divide (albumin/globulin) = > 1

  • Abnormal: When you lose albumin in the blood, ratio switches to <1 (inversion)
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37
Q

What happens if you do not have enough albumin in the tissue?

A

Albumins maintain oncotic pressure, if you don’t have enough -> the tissues will have a high oncotic pressure and pull fluid from the vessels into tissues

38
Q

What does Hypoalbuminemia lead to?

A

Generalized edema

39
Q

What is generalized edema characterized by?

A

Swelling of the face, particularly under the eyes:

  • Adrenal cortex is stimulated to increase aldosterone secretion, which causes increased absorption and pulling of fluid from the primary urine (anterior/medial portion of face, ankle low back, low abdomen (abdominal, pleural and heart cavity)
40
Q

If there is escape of albumin in the blood ________

A

Fluid will exit the vessels into the tissue (osmosis)

41
Q

What are the signs of Hypoalbuminemia?

A
  • Ascites
  • Pleural Effusion
  • Pericardial Effusion
  • Muehrcke’s lines aka M’s nails aka leukonychia striata
42
Q

What is Ascites?

A

Accumulation of transudate in the abdominal cavity

43
Q

What is Pleural effusion?

A

Accumulation of transudate fluid in the pleural cavity

44
Q

What is Pericardial Effusion?

A

Accumulation of transudate fluid in the pericardial cavity

45
Q

What are Muehrcke’s lines aka?

A

Muehrcke’s nails aka Leukonychia striata

46
Q

What are Muehrcke’s lines?

A

An appearance of horizontal lines beneath the nail and specific swelling of the nail bed

  • See lines in the nails parallel to lunula
47
Q

Where would you see Muehrcke’s lines?

A

With Nephrotic syndrome, especially Hypoalbuminemia

48
Q

In generalized edema during Nephrotic system, is transudate or exudate escaped?

A

Transudate

49
Q

What is Transudate?

A

Perfusion of the fluid portion of the blood which develops in edema (formation does not allow for escape of WBC’s, very little protein in the transudate fluid in tissues)

50
Q

What is (4) Hyperlipidemia and Lipiduria?

A

Albumin is produced in the liver (to meet the demand) as glycoproteins OR lipoprotein to increase the concentration of lipids in the blood -> loss of protein component

51
Q

What is the cause of (4) Hyperlipidemia and Lipiduria?

A
  • Lipid goes through the damaged glomerular membrane
  • Casts are formed with fat globules
  • It manifests and accumulates fluid in the pleural and abdominal cavity
52
Q

What will you see with Diabetic Nephropathy?

A

1) Glomerular lesions
2) Renal Vascular lesions
3) Pyelonephritis often with Necrotizing Papillitis

53
Q

What are Glomerular lesions associated with Diabetic Neuropathy?

A
  • Glomerular basement membrane thickening
  • Diffuse glomerulosclerosis (diffuse increase of mesangial cell proliferation)
  • Nodular Glomerulosclerosis (characterized by Kimmelstiel-Wilson lesions - ball like deposits of a laminar matrix within the masangium
54
Q

What are Renal Vascular lesions associated with Diabetic Nephropathy?

A
  • Hyaline arteriosclerosis of both afferent and efferent arterioles
  • Atherosclerosis
55
Q

What Primary Glomerular Diseases are associated with Nephrotic Syndrome?

A

1) Minimal change disease (lipoid Nephrosis) - droplets
2) Membranous GMN
3) Focal Glomerulosclerosis**** Major cause of nephrotic disease that leads to chronic GMN
4) . Membranoproliferative Glomerulonephritis (GMN)

56
Q

What are the Systemic Diseases associated with Glomerulonephritis?

A

1) . Diabetes Mellitus
2) . Amyloidosis
3) . SLE systemic lupus erthematosus

57
Q

What is Amyloidosis associated with Nephrotic syndrome?

A

Deposition of amyloid

  • Amyloid: The generic term for a variety of proteins does material that are abnormally deposited in tissue interstitium in a spectrum of clinical disorders
58
Q

What are the 2 types of Amyloidosis?

A

1) Amyloid AA

2) . Amyloid BB

59
Q

What does Amyloidosis lead to?

A

Amyloidosis is Idiopathic, incurable and leads to pressure atrophy

60
Q

What happens to functional tissue during Amyloidosis?

A

Normal functional tissue, in the KIDNEYS, BRAIN, SKIN, AND LIVER* is destroyed by intercellular deposition of amyloid

61
Q

What normally accompanies Amyloidosis?

A

Patients don’t live more than 2 years, and it is usually accompanied by AS and other autoimmune diseases

62
Q

What is Chronic GMN?

A

Typically the end stage of GMN that has slow progression - glomeruli are obliterated and replaced by CT - later the kidney will decrease in size and become granulated

63
Q

What does Chronic GMN lead to?

A

Slow inflammation which leads to loss of renal tissue and chronic renal failure

64
Q

What happens to the kidney in Chronic GMN?

A

The kidney becomes CONTRACTED* due to CT (becomes small, half of normal size, yellow, pale, and coarsely granular)

65
Q

What are the Symptoms of Chronic GMN in the GI system?

A

Waste products remain in the body, waste products being excreted = thin layer of frost

66
Q

What are the symptoms of Chronic Renal failure in the Circulatory system?

A

Fibrous structures like pericardium pericardium and pleura attempt to filtrate the products and cause an accumulation of crystals of toxic products and can cause the manifestation of bruits when auscultation

= FUNERAL BRUIT ***

  • Deposition of crystals into the pericardial cavity
67
Q

What happens to the Nervous System during Chronic Renal Failure?

A

Psychosis, paranoia hallucinations

68
Q

When would you develop Hematopoiesis?

A

With Chronic Renal Failure

  • non production of erythropoietin by the kidney (smell of urine in the mouth)
69
Q

What is the treatment for Chronic Renal failure?

A

Kidney Replacement: Patient dies without it

  • HEMODIALYSIS** : Used to prolong life when kidney isn’t functioning, lasts 8 hrs every other day
70
Q

What is the #1 cause of death in the US?

A

Cardiovascular problems

71
Q

Rheumatic fever aka

A

Migratory Arthritis

72
Q

Where is Rheumatic fever common in?

A

In the past that affected young people (teens)

73
Q

What does Rheumatic fever effect?

A

Joints, heart, Associated with strep throat** -> acute tonsillitis -> follicular strep throat beginning not cause

74
Q

What is the beginning of the of follicular strep throat?

A

Beta hemolytic streptococcus group A (pyogenesis)

75
Q

What is Molecular Mimicry associated with Rheumatic Fever?

A

After repeated strep throat episodes , antibodies created to fight the strep throat infection attach to the heart and destroy the tissue

76
Q

What is the pathogenesis of Rheumatic fever?

A

Tonsils (too cold water)

Infection: Beta hemolytic Step group A (same as GMN)

Repeated strep throat episodes

77
Q

What is the treatment for Rheumatic Fever?

A

Lacunar Tonsilits: Gargle with salt water

Follicular Tonsillitis: Must take antibiotics or tonsillectomy (but labile tissue, so might grow back)

78
Q

Strep Throat aka

A

Acute Tonsillitis

79
Q

What is strep throat aka acute tonsillitis ?

A

Common disease behind common cold

  • Inflammation of the pharynx and acute tonsillitis of the palatine tonsils (formation of pus) which eventually leads to the development of rheumatic fever
80
Q

Define Molecular Mimicry:

A

Pyogenes infection causes immune responses characterized by formation of antibodies against the antigens of the streptococcal wall - tissue of the heart has the same configuration as the streptococcal wall antigen — antibodies bind to both the S. Pyogenes and heart tissue - heart DESTROYED in phagocytic process

81
Q

Tonsillitis will eventually lead to ____

A

Development of RF - If you have relapse twice a year, must be removed -> removing the tonsils does not mean you will have more infections in the future

  • If not all removed = can regenerate
82
Q

If tonsils are not completely removed what do they become?

A

They can regenerate and become hypertrophic or hyper plastic

83
Q

WHat are the major provocative factors that lead to tonsillitis ?

A

Sudden changes in temperature: Exposure to cold (drinking cold water after overheated)

84
Q

What are the 2 types of tonsillitis?

A

1) Lacunar

2) FOllicular

85
Q

Define Lacunar Tonsillitis:

A

With regular inflammation of the tonsils, it becomes structure allows for pockets and spaces to be filled with bacteria

  • Grows in normal temp, pain is caused by swelling, infection in cracks, and forms pus (looks white)
86
Q

How do you remove white pus in Lacunar Tonsilitis?

A

Gargle salt water

87
Q

What is FOllicular Tonsillitis ?

A

The glands within the tonsils are infected, pus filled spots (cannot be removed mechanically) — inflammation makes it difficult to swallow (fever > 105) very dangerous

88
Q

How do you treat FOllicular Tonsillitis?

A

Antibiotic treatment is necessary, if don’t treat properly (with antibiotics) can develop chronic tonsillitis or repetition of tonsillitis -> GMN or RF

89
Q

What is Retrotonsillar abscess?

A

Development of suppurative inflammation (formation of pus behind the tonsils) which can go DOWN between layers of mediastinum

90
Q

What can Retrotonsillar abscess lead to?

A

Very dangerous (can lead to death) - if you see bulging of the posterior wall of the pharynx , this requires immediate action (cut off and pus drained)

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