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NBDE Part 1 > Systemic Pathology > Flashcards

Systemic Pathology Flashcards

1
Q

What are Teratogens?

A

Teratogenesis

  • Induction of nonhereditary congenital malformation (birth defects) in a developing fetus by exogenous factors:
    • Physical
    • Chemical
    • Biologic agents
  • Teratogens = Teratogenic agents
  • Maternal infection
    • TORCH complex:
      • Toxoplasmosis, Other agents, Rubella, CMV (cytomegalovirus) and HSV (Herpes Simplex Virus)
  • Physical agents
    • Radiation
    • Hypoxia
    • CO2
    • Mechanical trauma
  • Hormones:
    • Sex hormones
      • Corticosteroids
  • Vitamine deficincies
    • Riboflavin
    • Naicin
    • Folic acid
    • Vitamin C
  • Drugs
    • Mitomycin
    • Dactinomycin
    • Puromycin
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2
Q

What are the effects of teratogens, Mechanism of action, and susceptibility

A

Teratogenesis

  • Effects of teratogens:
    • Death
    • Growth retardation
    • Malformation
    • Functional impairment
  • Mechanism of teratogens
    • Specific for each teratogen: inhibit, interfere, or block metabolic steps critical for normal morphogenesis
    • Most are site or tissue-specific
  • Susceptibility to teratogens is :
    • Variable
    • Specific for each developmental stage
    • Dose-dependent
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3
Q

Name the Autosomal Abnormalities (chromosomal)

A

Down syndrome

Edward syndrome

Patau syndrome

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4
Q

What is Down syndrome?

A

Autosomal Abnormality

Down Syndrome

  • Chromosomal Abnormality: Trisomy 21
  • Findings:
    • Mental retardation
    • Epicanthal folds
    • Large protruding tongue
    • Small head
    • low-set ears
    • Broad flat face
    • Simian crease
    • Complications
    • Increased leukemia
    • Increased infection
    • Alzheimer-like brain change

Down syndrome is the most frequent chromosomal disorder (1:700 births). People with down syndrome can live into their 30s and 40s.

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5
Q

What is Edward syndrome?

A

Autosomal Abnormality

Edward syndrome

  • Chromosomal Abnormality: Trisomy 18
  • Findings:
    • Mental retardation
    • Small head
    • Micrognathia (small lower jaw)
    • Pinched facial appearance
    • Low-set, malformed ears
    • Rocker bottom feet
    • Heart defects
    • Prognosis: Months

Second most incidence: 1:3000

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6
Q

What is Patau Syndrome?

A

Autosomal Abnormality

Patau Syndrome

  • Chromosomal Abnormality: Trisomy 13
  • Findings:
    • Mental retardation
    • Microcephaly (Small head)
    • Microphthalmia (small eye)
    • Brain abnormalities
    • Cleft lip and palate
    • Polydactyly
    • Heart defects
    • Prognosis: < 1 yr

Least likely of the three autosomal abnormalities to occur

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7
Q

Name and describe the two types of Sex chromosome abnormalities

A

Sex Chromosome Abnormalities

Klinefelter Syndrome

  • Chromosomal Abnormality: XXY
  • Findings:
    • 1:500 men
    • Manifests at puberty
    • Hypogonadism, atrophic testes
    • Tall stature
    • Gynecomastia
    • Female pubic hair distribution
    • Low IQ
    • Associated with increased material and increased paternal age

Turner Syndrome

  • Chromosomal Abnormality: XO
  • Findings:
    • 1:3000 live female births
    • Diagnose at birth or puberty
    • Female hypogonadism
    • Primary amenorrhea
    • Short Stature
    • Webbed neck
    • Wide-spaced nipples
    • Coarctation of aorta
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8
Q

What are Lysosomal Storage Diseases

A

Lysosomal Storage Diseases

  • Are common in people of Eastern European ancestry
  • Diseases include:
    • X-linked
      • Fabry
      • Hunter’s
    • Autosomal Recessive
      • Tay-Sachs
      • Gaucher
      • Niemann-pick
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9
Q

Explain Cystic Fibrosis

A

Childhood Genetic Disorder

Cystic Fibrosis

  • Most common fatal genetic disease in white children
    • Due to the deletion causing loss of phenylalanine at position 508 in the CFTR gene
  • Occurs in both males and females (M = F)
  • Life expectancy = 28 yrs
  • Generalized exocrine gland dysfunction. Problem with Cl- transporter
  • Multiple organ systems
    • Characterized by respiratory and digestive problems
  • Pathogenesis: Chromosome 7q
    • Gene encodes CFTR (cystic fibrosis transmembrane regulator)
    • Regulates Cl- and Na+ transport across epithelial membranes
  • Affects Na+ channels, especially mucous and sweat glands
  • Tests: Sweat chloride test
  • Findings:
    • Chronic pulmonary disease
      • From thick mucous in airways
        • Lung infections (bronchiectasis)
        • Bronchiectasis
    • Pancreatic exocrine insufficiency
    • Meconium ileus
      • Intestinal obstruction in infants/newborns
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10
Q

What is von Hippel-Lindau Disease

A

Childhood Genetic Disorder

von Hippel-Lindau Disease

  • Autosomal Dominant
    • Chromosome 3
    • VHL gene
  • Findings
    • Hemangiomas (bloody red birthmark)
      • Retina
      • Cerebellum
  • Cysts and adenomas
    • Liver
    • Kidney
    • Adrenal glands
    • Pancreas
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11
Q

What is Marfan’s syndrome

A

Childhood Genetic Disorder

Marfan’s Syndrome

  • Uncommon hereditary connective-tissue disorder
    • Fibrillin gene mutation
  • Findings:
    • Skeletal
      • Tall and thin patients
      • Abnormally long legs and arms
      • Spiderlike fingers
    • Cardiovascular
      • Cystic medial necrosis of aorta
        • Risk aortic incompetence, dissecting aorta aneurysm
      • Distensible mitral valve
    • Ocular: Lens dislocation
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12
Q

State the two Hypopigmentation disorders of the skin and explain

A

Hypopigmentation Disorders

Albinism

  • Failure in pigment production from otherwise intact melanocytes
  • usually tyrosinase problem; can’t convert tyrosine to DOPA (in the pathway to form melanin)

Vitiligo

  • Acquired loss of melanocytes
  • Discrete areas of skin with depigmented white patches
  • May be autoimmune
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13
Q

State the disorders associated with Hyperpigmentation

A

Hyperpigmentation

  • Freckle (ephelis): increased melanin pigment within basal keratinocytes
  • Lentigo: Pigmented macule caused by melanocytic hyperplasia in epidermis
  • Pigmented nevi (benigh - nonneoplastic) skin lesion
  • Lentigo maligna (benign - nonneoplastic) skin lesion
  • Cafe au lait spots
    • Increase in melanin content with giant melanosomes
    • Conditions with cafe au lait spots include:
      • Neurofibromatosis type I (most frequent neurocutaneous syndrome)
      • McCune - Albright syndrome (Fibrous dysplasia)
      • Tuberous sclerosis (rare disease that causes nonmalignant tumors in the brain and organs)
      • Fanconi anemia (rare disease resulting in loss of DNA repair with increased risk of cancer and endocrine problems)
  • Diffuse hyperpigmentation with Addison’s disease (too little cortisol)
    • Secondary to increased melanocyte-stimulating hormone
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14
Q

State the type of Viral Skin Eruptions

A

Viral Skin Eruptions

  • Molluscum contagiosum (Poxvirus)
  • Verruca vulgaris (common wart) (Human papilloma virus (HPV))
  • Herpes simplex
  • Roseola (exanthema subitum) (herpes virus 6 and 7)
  • Rubella
  • Measles (rubeola) (paramyxovirus)
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15
Q

Describe Impetigo

Etiology

Signs/symptoms

Treatment

Course/prognosis

A

Impetigo

  • Common skin infection
    • Common in preschool age children (2-5 yrs old)
    • Especially during warm weather
  • Etiology
    • Invasion of epidermis by staphylococcus aureus or Streptocuccus pyogenes
    • Similar to cellulitis, but more superficial
    • Highly infectious
  • Signs/symptoms
    • Starts as itchy, red sore
    • Blisters -> breaks -> oozes
    • Ooze dries; lesion becomes covered with a tightly adherent crust
    • Grows and spreads circumfrentially (no deep); rarely impetigo forms deeper skin ulcers
    • Contagious; carried in the oozing fluid
  • Treatment
    • Topical antimicrobial (eg. bactroban)
    • Oral antibiotic (erythromycin or dicloxacillin) rapid clearing of lesions
  • Course/prognosis
    • Impetigo sores heal slowly and seldom scar
    • Cure rate is extremely high
    • Recurrence is common in young children

Note: Acute glomerulonephritis (renal disease) is an occasional complication (poststreptococcal glomerulonephritis (GMN))

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16
Q

Name the immunologic Skin Lesions

A

Immunologic Skin Lesions

Hives

Pemphigus Vulgaris

Bullous Pemphigoid

Erythema Multiforme

Steven-Johnson Syndrome

Toxic Epidermal Necrolysis

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17
Q

Explain the immunologic Skin Lesions

Hives

A

immunologic Skin Lesions

Hives

  • Urticaria = wheals
  • Type I hypersensitivity
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18
Q

Explain the immunologic Skin Lesions

Pemphigus Vulgaris

A

immunologic Skin Lesions

Pemphigus Vulgaris

  • Ages 30-60
  • Clinical
    • Oral mucousal lesions (often first sign)
    • Skin lesion follow
    • Bullae rupture, leaving raw surface susceptible to infection
  • Etiology
    • Autoimmune: IgG antibodies against desomsome protein
  • Histology:
    • Formation of interdermal bullae
      • Acantholysis: Tzanck cells
      • Basal layer intact
  • Immunofluorescence show encircling of epidermal cells
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19
Q

What are Tzanck cells?

A

Tzanch cells

Multinucleate giant cells caused by a variety of skin pathologies

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20
Q

Explain the immunologic Skin Lesions

Bullous Pemphigoid

A

Bullous Pemphigoid

  • Resembles pemphigus vulgaris
  • Clinically less severe
  • Etiology
    • Autoimmune: IgG antibodies against hemidesmosome proteins
  • Histology
    • Subepidermal bullae
    • Characteristic inflammatory infiltrate of eosinophils in surrounding dermis
    • Immunofluorescence shows linear band
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21
Q

What is the main difference between Pemphigus vulgaris and Bullous pemphigoid

A
  • Pemphigus vulgaris
    • Intraepidermal bullae
      • More superficial
  • Bullous pemphigoid
    • Subepidermal bullae
      • Deep under epidermis
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22
Q

Explain the immunologic skin lesion

Erythema Multiforme

A

immunologic skin lesion

Erythema Multiforme

  • Peak incidence second and third decades
  • Etiology
    • Type III hypersensitivity
    • Response to:
      • Medications
        • Sulfa drugs
        • penicillin
        • Barbiturates
      • Infection
      • HSV
      • Hycoplasma
      • Other illnesses
  • Damage to blood vessels of skin (because of immune complexes)
  • Clinical
    • Classic “target”, “bull’s-eye” or “iris” skin lesion
      • Central lesion surrounded by concentric rings of pallor and redness
      • Dorsal hands
      • Forearms
    • No systemic symptoms
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23
Q

What are the following immunologic skin lesions

  1. Steven-Johnson Syndrome
  2. Toxic Epidermal Necrolysis
A

immunologic skin lesions

1. Steven-Johnson Syndrome

  • Variant, more severe form of erythema multiforme
  • Severe systemic symptoms
  • Extensive skin target lesions
    • Involve multiple body areas, especially mucous membranes

2. Toxic Epidermal Necrolysis

  • Also called TEN syndrome and Lyell’s syndrome
  • Multiple large blisters (bullae) that coalesce, sloughing of all or most of the skin and mucous membranes
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24
Q

Name and describe the Benign (Nonneoplastic) skin lesions

A

Benign (Nonneoplastic) skin lesions

  1. Acanthosis Nigricans
    • Cutaneous finding of velvety hyperkeratosis and pigmentation
      • Flexural areas, most often (axilla, nape of nex, flexures, Anogenital region)
      • Often a marker of visceral malignancy (>50% have cancer: Gastric carcinoma, Breast, lung, uterine cancer)
    • Seen in diabetes
    • Histology:
      • Acanthosis, Hyperkeratosis, Hyperpigmentation
  2. Hemangioma
    • Hamartoma (not ture neoplasm)
      • Disorganized growth composed of tissue normally found in a given location
  3. Xanthoma
    • Associated with hypercholesterolemia
    • Clinical
      • Most common site:
        • Eyelids (xanthelasma)
        • Nodules over tendons or joints
      • Histology
        • Yellowish papules or nodules composed of
          • Focal dermal collections of lipid-laden histiocytes
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25
Q

What is the difference between hamartoma and choristoma?

A

Hamartoma = disorganized growht composed of tissue normally found in a given location

Choristoma = growth composed of histologically normal tissue found at a site where it is not normally found in the body

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26
Q

Explain Edema and how it is caused

A

Edema

  • Abnormal accumulation of fluid in intestinal spaces or body cavities
  • Fluid moves out of intravascular space
  • Results from some combination of:
    • Increased capillary permeability (with histamine)
    • Increased capillary hydrostatic pressure
    • Increased interstitial fluid colloid osmotic pressure
    • Decreased plasma colloid osmotic pressure
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27
Q

Name and describe the two types of Edema

A

Edema

  • Types of Edema:
    • Transudate
      • More watery (serious) edema fluid
      • Usually noninflammatory
      • From altered intravascular hydrostatis or osmotic pressure
    • Exudate
      • More protein-rich edema fluid
      • usually inflammatory
      • From increased vascular permeability (with inflammation)
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28
Q

Name and describe examples of Transudate

A

Examples of Transudate

  • Anasarca: Generalized edema
  • Hydrothorax: Excess serous fluid in pleural cavity
  • Hydropericardium: Excess watery fluid in pericardial cavity
  • Ascites (hydroperitoneum): Excess serous fluid in peritoneal cavity (stomach)
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29
Q

What does Right-sided conjestive heart failure lead to vs. Left-sided conjestive heart failure?

A
  • Right-sided conjestive heart failure
    • results in peripheral edema
  • Left-sided conjestive heart failure
    • results in pulmonary edema
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30
Q

What are examples of Edemas and causes

A

Edemas and causes

  • Congestive Heart Failure
    • Increase in plasma/capillary hydrostatic pressure
  • Nephrotic syndrome
    • Decrease in plasma oncotic pressure
  • Cirrhosis
    • Increase in capillary hydrostatic pressure
    • Decrease in plasma oncotic pressure
  • Elephantitis
    • Increase in plasma/capillary hydrostatic pressure
    • Secondary to decrease lymphatic return
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31
Q

What is Shock

A

Shock

Decreased cardiac output is the major factor in all types of shock (because either decrease HR, decrease Stroke Volume, or both)

  • Decrease tissue perfusion
  • Hemodynamic changes result in
    • Decrease blood flow, thereby
    • Decrease oxygen and metabolic supply to tissue
  • Can result in multiple organ damage or failure
  • Symptoms
    • Fatigue
    • Confusion
  • Signs
    • Cool pale skin (pallor)
    • Weak rapid pulse (tachycardia = icncrease HR)
    • Decrease BP (hypotension)
    • Decrease urine output
  • Shock requires immediate medical treatment and can worsen rapidly
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32
Q

What are the Major categories of shock

and describe

A

Major Categories of Shock

  • Hypovolemic
    • Decrease blood volume
      • Ex: Hemorrhage, Dehydration, Vomiting, Diarrhea
  • Cardiogenic
    • Pump failure, Usually Left ventrical failure, Sudden decrease in Cardiac Output
      • Ex: Massive MI, Arrhythmia
  • Distributive
    • Septic
      • Infection (endotoxin release), Gram negative bacteria, Causes vasodilation
        • Ex. Severe infection
    • Neurogenic
      • CNS injury, Causes vasodilation
        • Ex. CNS injury
    • Anaphylactic
      • Type I hypersensitivity, Histamine release, Vasodilation
        • Ex. Anaphylactic allergic reaction (insect sting)
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33
Q

Name and decribe the three stages of shock

A

Stages of Shock (decreased blood flow)

  • Nonprogressive (early)
    • = compensated
    • Increase sympathetic NS
    • Increase Cardiac Output
    • Increase Total periferal resistance
    • Try to maintain perfusion to vital organs
  • Progressive
    • Decrease cardiac perfusion
    • Cardiac depression
    • Decreased Cardiac output
    • Metabolic acidosis (Compensatory mechanism are no longer adequate)
  • Irreversible
    • Organ damage
    • Decrease high energy phosphate reserves
    • Death (even if blood flow is restored)
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34
Q

Describe Congestion (Hyperemia) and its types

A

Congestion (Hyperemia)

  • Increased volume of blood in local capillaries and small vessels
  • Active congestion (active hyperemia) increased arteriolar dilation (inflammation, blushing)
  • Passive congestion (passive hyperemia): decreased venous return (obstruction, increased back pressure)
    • Two forms:
      • Acute
        • Shock or right sided heart failure
      • Chronic
        • In lungs (usually secondary to left sided heart failure)
        • In liver (usually secondary to right sided heart failure)
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35
Q

What is Thrombosis

What is the difference between Arterial and Venous Thrombi

A

Thrombosis

  • Blood clot attached to endothelial surface (blood vessel or heart - endocardium)
    • usually a vein
    • Virchow’s triad
  • Arterial thrombi
    • Lines of Zahn (morphologically)
    • Alternating red and white laminations
  • Venous Thrombi
    • Propagate: enlarge while remaining attached to vessel wall
    • Embolize
    • Detach as large embolus
    • Fragment off as many small emboli; shower emboli
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36
Q

What is the Virchow’s Triad for Thrombosis

A

Virchow’s Triad for Thrombosis

  • Endothelial injury
  • Alteration in blood flow
  • Hypercoagulability of blood
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37
Q

What are the Lines of Zahn for Arterial thrombi?

A

Lines of Zahn (arterial thrombi)

  • White (fibrin and platelet) layers alternating with dark (RBC) layers
  • Indicated thrombosis in aorta or heart before death
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38
Q

That are the types of Thrombus

  • Name and describe
A

Types of Thrombus

Agonal

  • Intracardiac thrombi
    • After prolonged heart failure

Mural

  • Thrombus from endocardial surface (or endothelium of large vessel) protrudes into lumen of heart or large vessel)
  • Forms after
    • MI; damage to ventricular endocardium (LV most often)
    • Atrial fibrillation
    • Aortic atherosclerosis can cause cerebral embolism

White

  • Thrombus composed mostly of blood platelets

Red

  • Thrombus composed of RBCs (rather than platelets)
  • Occurs rapidly by coagulation with blood stagnation

Fibrin

  • Thrombus composed of fibrin deposits
  • Does not completely occlude the vessel
39
Q

What are the predisposing factors to thrombosis

Both Atrial and Venous thrombosis

A

predisposing factors to thrombosis

  • Atrial Thrombosis
    • Atherosclerosis (major cause)
  • Venous Thrombosis
    • Heart failure
    • Tissue damage
    • Bed rest (immobilization)
    • Pregnancy
    • Oral contraceptive pills
    • Age
    • Obesity
    • Smoking
40
Q

What are Embolus

A

Embolus

  • Intravascular mass
    • Solid, liquid, gas
  • Travels within a blood vessel
    • Lodges at distant site
    • Occludes blood flow to vital organs
    • Possibly leads to infarction
  • Thromboemboli (most common): blood clot
    • Breaks off existing thrombus
    • Forms and is released downstream in the circulation (eg. from heart chambers in atrial fibrillation)
  • Fat embolism: Especially in long bone fracture
  • Gas embolism: air into circulation (eg. Caisson disease)
  • Amniotic fluid embolism: With delivery; can activate diffuse/disseminated intravascular coagulation (DIC)
  • Tumor embolism
41
Q

Pulmonary Embolism

A

Pulmonary Embolism

  • Embolism causing pulmonary artery obstruction
  • Usually arises from
    • Deep vein thrombosis (DVT); usually from lower extremeties (above popliteal fossa)
  • Course
    • Systemic vein
    • Right heart
    • Pulmonary artery
  • Causes
    • Right heart strain
    • Possible infacrtion in the affected segment
    • Possible pleurisy (pleuritic chest pain)
  • Predisposing factors
  • Virchow’s triad
    • Especially immobilization (leading to stagnation)
    • Thrombophlebitis (inflammation of veins related to blood clot)
    • Hypercoagulable states
42
Q

Explain Artheriosclerosis and Atherosclerosis

A

Arteriosclerosis

  • Hardening of the arteries
  • General term for several diseases causing changes to artery wall:
    • Thicker
    • Less elastic

Atherosclerosis

  • Degenerative changes in artery walls
  • Most common cause of arteriosclerosis
    • _​​_Most important contributor to arterial thrombosis
    • Most susceptible arteries = aorta and coronary arteries
  • Atherosclerostic plaques: Fatty material accumultating under the arterial walls inner lining
  • Occurs in arteries (no veins)
  • Risks
    • Men and postmenopausal women (estrogen = protective)
    • Smoking, Hypertension, Hereditary (Familial hypercholesterolemia), Nephrosclerosis, Dibetes, Hyperlipidemia
  • Sites
    • Carotid, coronary, Circle of willis, Renal and mesenteric arteries
  • Can lead to:
    • Ischemic heart disease (CAD)
    • Heart attack (myocardial infarction (MI))
    • Stroke or aneurysm formation
  • Pathogenesis:
    • Fatty streak
      • Foam cells in intima (lipid laden macrophages)
    • Atheromas
      • Cholesterol, Fibrous tissue, Necrotic, debris, Smooth muscle cells
  • Complications
    • decreased elasticity of vessels
    • Ulceration of plaque; predisposing to thrombus formation
    • Hemorrhage into the plaque;narrowing lumen, possibly occluding blood flow
    • Thrombus formation
    • Embolization; overlying thrombus or plaque material itself
  • Symptoms
    • Depend on sites
      • Visual changes, dizziness; Carotid or intracerebral arteries
      • Angina: Coronary arteries
      • Leg pain (claudication): lower extremity arteries
43
Q

What is Familial hypercholesterolemia?

A

Familial hypercholesterolemia

  • Autosomal dominant diseae
  • Anomalies of LDL (low-density lipoprotein) receptors
  • Atherosclerosis and its complications
    • Xanthomas
    • MI by age 20
44
Q

What are the two types of Hypertension and explain

A

Hypertension = silent killer (asymptomatic)

Primary (Essential) Hypertension

  • Accounts for 90-95% of hypertension
  • No identifiable cause; related to increased Cardiac Output and increased Total Peripheral Resistance
  • Risks
    • Genetic
      • Family history, African Americans
    • Environment
      • Incresed dietary salt intake, Stress, Obesity, Cigarette smoking, Physical inactivity
  • Pathologic findings
    • Hypertrophy of arteries and arterioles NOT capillaries (because no smooth muscle)
    • Increase wall to lumen ratio
      • Increased smooth muscle cell growth (because increased pressure, stretch)
    • Decreased arteriolar and capillary density
    • Decreased total cross-sectional area of capillaries and arterioles
  • Three organs most often damaged:
    • Heart : 60% die due to complications
    • Kidney : 25% die due to renal failure
    • Brain : 15% die due to stroke or neurologic complications

Secondary Hypertension (related to another disease)

  • Hypertension (HTN) from known causes
    • 5-10% of HTN cases
    • Identifiable, often correctable cause
  • Renal disease
    • Most common cause of secondary hypertension
    • Renin-angiotensin-aldosterone system
    • Two categories
      • Renal parenchymal diseases
      • Renal artery stenosis
  • Endocrine Disorders
    • Hyperaldosteronism (Conn syndrome)
    • Cushing syndrome
    • Hyperthyroidism
    • Diabetes
    • Pheochromocytoma
  • Other causes:
    • Coarctation of the aorta
    • Preeclampsia/eclampsia/toxemia of pregnancy
      • Preeclampsia:
        • Occurs in pregnant patients
        • Hypertension: > 140 systolic, or >90 diastolic after 20 weeks gestation
        • Proteinuria
        • Edema
45
Q

What is an Aortic Aneurysm and Aortic Dissection

A

Aortic Aneurysm

  • Abnormal, localized dilation of the aorta
  • True aneurysm = dilation of all three layers (intima, media, adventitia)
  • Causes
    • Atherosclerosis
    • Cystic medial necrosis
      • Marfan
      • Ehler-Danlos
    • Infectious aortitis
      • Syphilitic aortitis
    • Vasculitis
  • Risk: RUPTURE

Aortic Dissection

  • Most often ruptures into the pericardial sac (hemopericardium) causing fatal tamponade
  • Blood in media layer of aorta
46
Q

Explain The types of Infections of the heart

A

Infections of the heart

  • Pericardium
    • pericarditis
  • Myocardium
    • myocarditis, often viral
  • Endocardium and heart valves
    • Endocarditis, often bacterial or inflammatory
47
Q

What is Endocarditis

A

Endocarditis

  • Inflammation of endocardium and/or heart valves
  • Symptoms: Develop quickly (acute) or slowly (subacute)
    • Fever (hallmark)
    • Nonspecific constitutional signs, Fatigue, Malaise, headache, Night sweats
  • Findings
    • Murmur (secondary to vegetations); may change with time
    • Splenomegaly
    • Splinter hemorrhages (small dark line) under fingernails
48
Q

What are the three types of Endocarditis?

A

Endocarditis

Infective

  • Usually bacterial
    • ​​Acute Endocarditis: Staph. aureus (50%) and secondary infection to somewhere else in body (IV drug users)
    • Subacute (Bacterial) Endocarditis: Strep. viridans (>50%). Patients with preexisitng valve disease
  • Intrinsic bacteremia
    • dental, Upper respiratory, Urologic, Lower GI, Introduced bacteremia, IV drug users (tricuspid valve)
  • Valvular involvement
  • Vegetations
    • Mitral
    • Tricuspid (IV drug users)

Rheumatic

  • Complication of rheumatic fever
    • Acute inflammatory disease (after streptococcal infections, age 5-15 yrs)
    • Type III hypersensitivity
  • Mitral valve most often calcification:
    • Stenosis, Insufficiency, both
  • Pathology: Aschoff bodies
  • Findings/criteria for diagnosis = Jones criteria
  • Rheumatic carditis usually disappears within 5 months. However, permanent damage to heart/heart valves usually occur, leading to rheumatic heart disease

Libmann-Sacks

  • Occurs in SLE (Systemic lupus erythematosus = autoimmune disease)
  • Nonbacterial endocarditis
  • Mitral valve most often small vegetations on either or both surfaces of valve leaflets
49
Q

What is Coronary artery disease (CAD)?

A

Coronary Artery Disease (CAD)

  • CAD = narrowing of coronary arteries
    • Atherosclerosis plaques
    • Decreased blood supply to myocardium
      • Decreased O2 and nutrients to myocardium
  • Consequences
    • Ischemia, Infarction
  • Symptoms
    • Classic symptom of CAD = angina = ischemia
      • Infarction (MI = heart attack with ECG changes and enzymes released from infarcted myocardial tissue)
50
Q

What is Angina and explain the types

A

Angina

  • Squeezing (tight) substernal chest discomfort; may radiate to:
    • left arm
    • neck
    • Jaw
    • Shoulder blade
    • Caused by decreased myocardial oxygenation
    • Atherosclerotic narrowing
    • Vasospasm
  • Types:
    • Stable Angina
      • Most common type
      • coronary artery disease (CAD)/atherosclerotic narrowing
      • Precipitated by exertion
        • Relieved by rest or nitrates
    • Unstable Angina
      • Occurs even at rest
      • More severe CAD
      • Often imminent MI
    • Primzmetal Angina
      • Intermittent chest pain at rest
      • Vasospasm
51
Q

What is a Myocardial infarction and what are the types

A

Myocardial Infarction

  • Most important cause of morbidity from CAD
  • Prolonged interruption of coronary blood flow to myocardium; coagulative nerosis
  • Cause: usually thrombus formation in the setting of a ruptured, unstable plaque
  • Types:
    • Complete Occlusion
      • Transmural infarction
      • ST elevation MI
    • Partial Occlusion
      • Subendocardial infarction
      • Non-ST elevation MI
  • Symptoms
    • Angina (that does not remit), sweating, nausea, stomach upset
  • Signs
    • ECG changes (ST elevation, ST depression, T waves, Q waves)
    • Enzyme leak
  • Prognosis
    • Good (if patient reaches hospital)
  • Compliations
    • Arrhythmia, Myocardial (pump) failure, cardiac rupture, papillary muscle rupture, ventricular aneurysm
52
Q

Where is Creatine phosphokinase (CPK) enzyme found in?

A

CPK: Enzyme found in (increases when damage to):

Heart

Brain

Skeletal muscle

NOT found in the liver….

53
Q

What is heart failure

A

Heart Failure

  • Heart’s ability to pump does not meet needs of the body
  • usually a chronic progressive condition
  • Can occur suddenly
  • Causes: Secondary to heart muscle damage
    • After MI
    • Cardiomyopathy
    • Valvular diseases
  • Signs and symptoms (Left and Right side heart failure)
    • Left heart failure
      • Exertional dyspnea, Fatigue, Orthopnea, cough, cardiac enlargement, Gallop rhythm (S3 or S4), pulmonary venous congestion
    • Right heart failure
      • Elevated venous pressure, Hepatomegaly, Dependent edema
        • usually caused by left side failure
        • Isolated RHF = uncommon
        • When right HF occurs: Corpulmonale
          • lung disease due to pulmonary hypertension
          • increased pulmonary vascular resistance causing increased R heart strain
        • RHF leads to systemic venous congestion and peripheral edema
  • Two earliest and most common signs of heart failure:
    • Exertional dyspnea (labored breathing)
    • Paroxysmal nocturnal dyspnea (coughing at night)
54
Q

Explain Cardiovascular Pulmonary Cross-correlation of Carbon monoxide (CO) poisoning and Pulmonary Edema

A

Cardiovascular Pulmonary Cross-correlation

Carbon Monoxide (CO) poisoning

  • Symptoms
    • Cherry-red discoloration of skin, mucosa, and tissues
    • Mental status changes
    • Coma -> death
    • (Cyanide poisoning poisons oxidative phosphorylation)
      • Mild poisoning: Presents with exhaustion and symptoms similar to a common cold or flu, delaying diagnosis

Pulmonary Edema

  • Fluid in alveolar space of the lungs (decrease O2 exchange)
  • Cause
    • usually left heart failure (increase hydrostatic pressure)
      • Fluid extravasation into lung spaces
      • Increased intracapullary hydrostatic pressure (heart failure)
      • Increased capillary permeability (Acute respiratory distress syndrome (ARDS)
  • Mechanism
    • Backlog of blood in left heart (increase volume)
    • Increased left heart pressure
    • Incresaed pressure in pulmonary veins (transmitted backward from heart)
  • Symptoms
    • Shortness of breath (SOB)/dyspnea
    • Orthopnea, cough, tachypnea, dependent crackles, tachycardia, neck vein distention
  • Treatment
    • Decreased vascular fluid (Diuretic)
    • Increased gas exchange and ehart function
      • O2, Antihypertensive, Positive inotropic agents, antiarrhythmics
  • Primary Pulmonary Hypertension:
    • Not known heart or lung diseases
    • Unknown etiology
  • Secondary pulmonary hypertension
    • Most common form
      • COPD (most often)
      • Left to right shunt
      • Increased pulmonary resistance
        • Embolism
        • Vasoconstriction from hypoxia
      • Left heart failure
  • Pulmonary hypertension can lead to Righ Ventrical hypertrophy and R heart failure (corpulmonale)
55
Q

What is Angina Pectoris?

A

Angina Pectoris

  • Occurs when the heart’s demand for oxygen is greater than the supply
  • Stable Angina
    • Most common form
    • Repeating patterns of chest pain with no change in character, frequency or intensity
    • Precipitated by exertion and relieved by rest or vasodilators such as nitroglycerin
  • Unstable Angina
    • Variable chest pain
    • Prolonged/recurrent pain at rest
    • Often indicates an MI is about to occur
  • Prinzmetal’s/Variant Angina
    • Caused by a vasospasm that narrows the coronary artery and lessens blood flow to the heart

Intermittent chest pain at rest

56
Q

Mechanisms of Asthma Precipitation

A
  • Allergic (immune) = Extrinsic
    • Type I hypersensitivity
      • Atopic asthma
        • IgE vs. allergin (IgE crosslink)
        • Fc binds mast cell
          • Mast cell degranulate:
            • Histamine
      • Causes: bronchospasm/inflammatory
  • Intrinsic (nonimmune) = Intrinsic
    • Direct Bronchoconstriction Release
      • Caused by chemical inhalation or medication
    • Increased Vagal stimulation
      • Respiratory threshold to vagal stimulation is lowered by
        • Viral infection
        • URIs (cold or flu)
      • Parasympathetics activity causes bronchoconstriction
  • COX Inhibitors (NSAIDs, ASA)
    • Cyclooxygenase pathway blocked
      • Arachidonic acid metabolism
    • Causes:
      • Increased leukotrienes
      • Bronchoconstrictors (as opposed to prostaglandins = bronchodilators)
57
Q

What is Chronic Obstructive Pulmonary Disease (COPD) and what are the two categories

A

Chronic Obstructive Pulmonary Disease (COPD)

  • Group of lung diseases characterized by increased airflow resistance
    • Emphysema
    • Chronic bronchitis
  • Types:
    • Obstructive Lung Diseases (Increase TLV)
      • Asthma
      • COPD
        • Emphysema = Pink Puffer
        • Chronic bronchitis = Blue Blower
    • Restrictive Lung Diseases (decrease TLV)
      • Intrinsic lung diseases:
        • Pneumoconioses
        • Sarcoidosis
        • Idiopathic pulmonary fibrosis
      • Extrinsic lung diseases
        • Kyphosis
        • Obesity
        • Neuromuscular weakness
58
Q

Explain Emphysema and state the types

A

Emphysema (COPD)

  • “Pink puffer”
  • Adults, usually smokers
  • Types of Emphysema
    • Centrilobular
      • Cigarette smoking
      • Upper lobe of lungs
    • Panlobular
      • Familial antiproteinase deficiency
      • Upper and lower lobes
  • Pathology:
    • Destruction of elastic fibers in alveolar wall
      • Decrease elastic recoil
        • Distal airspaces enlarged (dilated alveoli) with inhalation
        • Lungs overexpand (increased total lung capacity)
      • Decreased radial traction (airways collapse w/exhalation)
        • leaving air behind, air trapped
      • Decreased functional parenchyma
  • Microscopic
    • Enlarged air spaces, broken septae projecting into alveoli (no fibrosis)
  • Clinical
    • Pink puffer
    • Dyspnea - labored breathing
    • No productive cough
      • Scant clear mucoid sputum production
      • Increased infection suscepibility
  • Findings: PO2 = normal
    • No cyanosis (they are pink)
    • Barrel chest
  • Pulmonary function test (PFTs)
    • Increased TLC = total lung capacity
    • Increased residual volume (RV)
    • Decreased FEV1/FVC (forced expiratory volume in 1 second/forced vital capacity)
  • Damage worsens with time = continue smoking
59
Q

What are restrictive lung diseases signs/lung affect

A

restrictive lung diseases

Decreased lung compliance

Decreased all lung volumes

Increased FEV1/FVC

= forced expiratory volume in 1 second/forced vital capacity

Discussed Diseases of Restriction:

Intrinsic lung diseases (Pneumoconiosis, Sarcoidosis)

Extrinsic lung diseases (Obesity, Kyphosis, NM weakness)

60
Q

What are the mechanisms of airway obstruction

A

airway obstruction

  • Airway hyperreactivity (bronchoconstriction): Asthma
  • Decreased elastic recoil (airways collapse): Emphysema
  • Increased Mucous: Chronic bronchitis

Discussed Diseases of Obstruction:

Asthma

COPD (Emphysema, Chronic Bronchitis)

61
Q

Explain Chronic Bronchitis (COPD)

A

Chronic Bronchitis (COPD)

  • “blue bloaters”
  • Adults with history of cigarette smoking
  • Definition: chronic productive cough for at least 3 months of the year for 2 yrs
  • Microscopic
    • Mucous hypersecretion
      • Bronchi: Hypertrophy of mucous glands and smooth muscle
      • Smaller airways: Goblet cell hyperplasia
    • Increased Reid index
      • increased ratio mucous gland thickness: bronchial wall thickness
  • Clinical
    • Productive cough (increased sputum)
    • Wheezing
    • Auscultation
      • Noisy chest
      • Rhonchi
  • FIndings: Decreased PO2 - Cyanosis (looks blue)
  • Complications:
    • Pulmonary hypertensition
      • RV overlaod; corpulmonale (RHF)
      • peripheral edema (bloaters)
    • Increased lung cancer risk (bronchogenic carcinoma) -> squamous metaplasia
62
Q

What are the following:

  • Atelectasis
  • Anthracosis
  • Silicosis
  • Asbestos
A
  • Atelectasis = lung collapse (alveolar collapse)
    • causes: Failure of expansion, Bronchial obstruction, External compression
    • Atelectasis neonatorum = alveolar collapse in newborn, usually due to decreased surfactant (premature infants)
  • Anthracosis
    • Coal workers pneumoconiosis = black lung disease
  • Silicosis = Most common and most serious pneumoconiosis (inhalation of silica)
    • Silica dust in alveolar macrophages
    • Thick pleural scars
    • Increased susceptibility to Tb (silicotuberculosis)
  • Asbestos
    • Inhalation of asbestos fibers
    • Can develop 15-20 yrs after exposure
    • Results in diffuse interstitial fibrosis
    • Findings: Ferruginous bodies (yellow-brown)
      • Stain with prussian blue
63
Q

What is Sarcoidosis?

A

Sarcoidosis

  • Unknown etiology
  • Diagnosis/biopsy; noncaseating granulomas
  • Black females: manifests in teens or younger adult years
  • Findings:
    • Interstitial lung disease
    • Enlarged hilar lymph nodes
    • Uveitis
    • Erythema nodosum
    • Polyarthritis
    • Hypercalcemia
  • Pathology
    • Noncaseating granulomas
      • Schaumann and asteroid bodies
  • Clinical
    • Bilateral hilar lymphadenopathy on CXR
    • Interstital lung disease (restrictive lung disease)
      • Cough/Dyspnea
    • Skin findings
64
Q

What is Mesothelioma

A

Rare tumor

involves parietal or visceral pleura

Associated with asbestos exposure: 25-45 year latency

Diffuse lesion; spreads over lung surface

65
Q

Explain Pneumonia

A

Pneumonia

  • Lung infection
    • Bacterial, Viral, Fungi
  • Clinical:
    • Fever, chills, productive cough, Blood-tinged sputum, Dyspnea, Chest pain
  • Findings
    • Hypoxia
    • Infiltrate on CXR
    • Crackles, other noises on auscultation
66
Q

Name the types of Pneumonia

Causes, Findings, Age

What is the difference between Viral and Bacterial Pneumonia?

A

Types of Pneumonia

  • Lumbar pneumonia
    • Cause:
      • Pneumococcus
        • Streptococcus pneumoniae
    • Findings: Exudate within alveolus, Consolidation, Lobe or entire lung
    • Age: Middle age
  • Bronchopneumonia
    • Cause:
      • Staph. aureus
      • Haemophilus influenzae
      • Klebsiella
      • Strep. pyogenes
    • Findings: Bronchiole and alveolar infiltrates, Patchy, 1+ lobe
    • Age: Infants and elderly
  • Interstitial pneumonia
    • Cause:
      • Viruses: RSV and adenovirus
      • Mycoplasma
      • Legionella
    • Findings: Diffuse patchy infiltrates (within interstitum), 1+ lobe
    • Age: Young Children

Viral Pneumonia:

  • Most common cause of pneumonia in young children
  • Peaks between age 2 and 3 yrs

Bacterial Pneumonia

  • Most serious pneumonias (typically)
  • Pneumococcus (strep. pneumo) is the most common cause
  • Most common fatal infection in the hospital
67
Q

What is a lung abscess and what is the most common predisposing factor?

A

Lung Abscess

  • Localized collection of pus in lungs
  • Causes:
    • Aspiration
      • Altered mental status
    • Bronchial obstruction
      • Cancer, pneumonia, bronchiestasis
    • Septic emboli
    • Most common predisposing factor = alcoholism -> in particular, aspiration (fluid to lungs bringing bacteria with it from oral cavity)
  • Organisms
    • Staphylococcus (most common)
      • other organisms:
        • Pseudomonas
        • Klebsiella (alcoholics)
        • Proteus
        • Anaerobes
  • Clinical
    • Productive cough; large amounts of foul-smelling sputum
    • Fever
    • Dyspnea
    • Chest pain
    • Cyanosis
    • Chest x-ray with fluid filled cavity
68
Q

What is Hemoptysis

and when does it occur

A

Hemoptysis

Coughing up blood (or blood-streaked sputum)

  • Respiratory infections (minor URIs)
  • Bronchitis
  • TB
  • Pneumonia
  • Bronchogenic carcinoma
  • Idiopathic pulmonary hemosiderosis (iron in lungs)
69
Q

What is Tuberculosis (TB)?

A

Tuberculosis (TB)

  • Worldwide condition
  • Increased in conditions of
    • Poor sanitation
    • Poverty
    • Overcrowding
  • Mycobacterium TB
    • Acid-fast bacilli
    • Strict aerobe
  • Transmitted by aerosolized “droplets”
  • Pathology
    • granuloma
      • giant cell
      • caseous necrosis
  • Clinical
    • Hemoptysis, weight loss, night sweats, Malaise, weakness
70
Q

Name the three types of Tuberculosis (TB), what sites they are found and characteristics

A

Types of Tuberculosis

  • Primary TB
    • Site:
      • Between upper and middle lobes
      • Lower part of upper lobe or upper part of lower lobe
    • Characteristics
      • Ghon’s complex
        • Parenchymal lesion(Calcified primary lesion + lymph node (LN) involvement)
        • Hilar LN’s
  • Secondary TB
    • Site: Lung apices (high O2 tension)
    • Characteristic: Reactivation of Ghon’s complex
  • Miliary TB
    • Site: Widely disseminated (spread)
    • Characteristics:
      • Lesions like “millet seed”
      • Multiple extrapulmonary sites

Clinical presentation:

  • Usually secondary TB, only 5% patients that have have primary TB have symptoms
  • Secondary TB = reactivation of the primary Ghon’s complex, which has remained quiescent (subclinical) and /or occurs years earlier

Pott’s disease = TB involving the vertebral body

71
Q

What is Ghon’s complex?

A

Ghon’s complex

= calcified primary lesion + lymph node involvement

Seen in Primary TB and reactivated in Secondary TB

72
Q

What is Mallory-Weiss Syndrome?

A

Mild to major bleeding (usually painless) at distal esophagus due to tears in the epithelium, proximal stomach

Most common in Men>40, Alcoholics, Hiatal hernia

Vomiting of blood (hematemsis) seen

73
Q

What is the following:

  • Achalsia
  • Hiatal hernia
  • Gastroesophageal Reflex Disease (GERD)
  • Esophageal Ulcers

What is the Zollinger-Ellison triad?

A
  • Achalsia
    • Decreased propulsion of food down the esophagus (decreased peristalsis)
    • Failure of LES to relax
    • Nerve related cause to smooth muscle
  • Hiatal hernia
    • Protrusion of part of the stomach through diaphragm into the thoracic cavity
  • Gastroesophageal Reflex Disease (GERD)
    • Acid reflex
    • Backflow of acidic stomach contents up into esophagus (LES leaky)
    • Risks: Hiatal hernia, Scleroderma
    • Symptoms: heartburn, Regurgitation of food, Hoarse voice, wheezing, coughing
    • Treatment: Proton pump inhibitor, Antacids
    • Complications
      • Can lead to Barrett’s esophagus (premalignant)
        • Type of metaplasia
        • Changes from squamous cell to columnar epithelium
        • Complication of chronic heartburn
  • Esophageal Ulcers
    • Erosion on the esophageal lining mucosa
    • usually caused by repeated regurgitation of stomach acid (HCL) to lower part of esophagus
    • Can also get esophageal infections causing erosion (candidal or viral)

What is the Zollinger-Ellison triad?

  • Increased gastric acid
  • Peptic ulcers
  • Panreatic gastrinoma
74
Q

What is Peptic Ulcer Disease (PUD)

A

Peptic Ulcer Disease (PUD)

  • Erosion in the lining of the stomach or duodenum
  • Circumscribed lesions in the mucous membrane
  • Occurs mostly in men aged 20-50
  • ~80% duodenal ulcers
  • Hemorrhage is the most common complication of PUD.
  • Causes:
    • Imbalance between acid and mucosal protection
      • NSAIDs (decrease mucosal protection: decreased prostaglandins)
      • Acid hypersecretion (Zollinger-Ellison)
    • Infection
      • Helicobacter pylori
  • Risks
    • Asprin, NSAIDs, Cigarette smoking, Older age
  • Symptoms: Pain
  • Complications:
    • Bleeding
      • When erode deep into blood vessels, Bleeding ulcers
    • Perforation (causes acute peritonitis)
  • Malignant change = uncommon
  • Treatment = antibiotics, anticid medications, proton pump inhibitors
75
Q

Hematemesis

A

Hematemesis

  • Vomiting of bright red blood, indicating rapid upper GI tract bleeding
  • Assoicated with esophageal varices (common in alcoholics) or peptic ulcers
76
Q

What are the following that are associated with

Small and Large Intestines

  • Meckel Diverticulum
  • Intestinal Lymphangiectasia
A

Small and Large Intestines

  • Meckel Diverticulum
    • Most common congenital anomaly of the small intestine
    • Remnant of embryonic vitelline duct
    • Located in distal small bowl
    • May contain ectopic gastric and duodenal, colonic, or pancreatic tissue
  • Intestinal Lymphangiectasia
    • In children, young adults in which lymph vessels supplying lining of small intestine becomes enlarged; fluid retention is massive
77
Q

What are the following that are associated with

Small and Large Intestines

Inflammatory Bowl Disease (describe breakdown of the two types)

A

Inflammatory Bowl Disease

  • Crohn’s and ulcerative colitis (UC)
  • Both can present with:
    • Abdominal pain
    • Obstruction
    • Bloody diarrhea (occult or gross)

Crohn’s Disease

  • Can affect entire GI from mouth to anus
    • Cobblestone appearance
    • Transmural inflammation (giant cell)
  • Chronic inflammation of the intestinal wall
  • Non-necrotizing granulomatous inflammation with ulcers, strictures and fistulas
  • No known cause and no cure

Ulcerative Colitis

  • Only the colon
    • Inflammation limited to mucosa and submucosa
  • Increased risk of secondary malignancy
78
Q

Explain Malabsorption syndromes and state the types and what the do

A

Malabsorption Syndromes

  • Nutrients from food are not absorbed properly
  • Not absorbed across small intestine into the blood
  • Clinical:
    • Children: Growth retardation, failure to thrive
    • Adults: Weight loss
  • Types:
    • Celiac disease:
      • Causes: Autoimmune disease triggered by gluten protein
      • Comments: Child or adult. Increase risk of GI lymphoma. MALToma
    • Tropical sprue
      • Cause: unknown, Probably infection
      • Comments: Travelers to the tropics, Steatorrhea (fatty diarrhea), Diarrhea, Weight loss, sore tongue (dec. vit B)
    • Whipple’s disease
      • Cause: Tropheryma whippelii
      • Comments: Middle-aged men, Slow onset of symptoms
        • Skin darkening
        • Inflamed painful joints
        • Diarrhea
          • Can be fatal
79
Q

Explain Pancreatitis

A

Pancreatitis

  • Inflammation of infection of the pancreas​
    • Severe mid-abdominal pain
    • Obstruction of the pathway of secretion of pancreatic enzymes into the intestine -> enzymes act on pancreas instead
    • Associated with alcoholism (chronic) and biliary disease/gallstones (acute)
  • Cause:
    • Injury to pancreatic cells
    • Obsruction of normal pancreatic outflow
      • Autodigestion/autolysis by pancreatic enzymes
    • Chronic cases, inflammation and fibrosis cause destruction of functional glandular tissue
  • Symptoms:
    • Severe Mid-adominal pain, destruction of pancrease
  • Laboratory:
    • Increase Lipase (important)
    • Increase amylase
  • Acute Pancreatitis:
    • Causes: Gallstones (#1), other biliary disease, Trauma, Cystic fibrosis in children
    • Symptoms: Abdominal pain, knifelike, radiation to back, Nausea and vomitting, Jaundice (if gallstone), pale/clay colored stool
    • Complication: Enzymatic hemorrhagic fat necrosis w/calcium soap formating with resultant hypocalcemia
  • Chronic pancreatitis:
    • Causes: Alcoholism (most often), hyperlipidemia, hyperparathyroidism
    • Symptoms: Abdominal pain, nausea, vomiting, fatty stool
    • Complications: pseudocyst, Pancreatic abscess, ascites
80
Q

Explain Cholelithiasis

A

Cholelithiasis

  • Stones in the gallbaladder = gallstones = jaundice
  • Choledocholithiasis = gallstones in the common bile duct (CBD)
    • result in obstructive jaundice, with yellow skin color caused by bile pigments being deposited in the skin
81
Q

Explain Cholesterolosis and

Gallbladder Diverticulosis

A

Cholesterolosis

  • Called strawberry gallbaladder
  • Small yellow cholesterol flecks against a red background in the lining of the gallbladder
    • Polyps may form insde GB

Gallbladder Diverticulosis

  • Small fingerlike outpouches of the GB lining may develop as a person ages; may cause inflammation and require GB removal
82
Q

What is Cirrhosis (of liver)

Characteristics

Cause

Clinical findings/complications

A

Cirrhosis (of liver)

  • Most common chronic liver disease
    • assicoated with increase in hepatocellular carcinoma
  • Occurs twice as often in males as in females
  • Third most common cause of death among people aged 45-65 (behind heart disease and cancer)
  • Characteristics:
    • Scarring/fibrous
    • Loss of hepatic architecture
    • Formation of regenerative nodules
  • Cause
    • Alcoholism (75%)
    • Viral hepatitis (Hep B, C)
    • Hemochromatosis
    • Wilson disease
      • Hepatolenticular degeneration - hereditary accumulation of copper in liver, kidney, brain, and cornea (green pigment in cornea)
    • Drugs/toxic injury, Biliary obstruction, Other inborn errors of metabolism (Galactosemia, Glycogen storage disease, Alpha-1 antitrypsin deficiency)
  • Clinical Findings
    • Ascites (accumulation of fluid in the peritoneal cavity, causing abdominal swelling)
    • Splenomegaly
    • Jaundice
    • Coagulopathy/bleeding disorders
    • Confusion/hepatic encephalopathy
    • Portal Hypertension (and its complications)
    • Esophageal varices (with hematemesis)
83
Q

What is Portal Hypertension

Characteristics

Cause

Clinical findings/complications

A

Portal Hypertension

  • Abnormally high blood pressure in the portal vein/system
  • Factors increase BP in portal vessels
    • Decrease volume of blood flow through the portal system
    • Increase resistance to blood flow through the liver
      • **Splenomegaly = most important sign of portal hypertension **
  • Causes
    • Cirrhosis of liver = most common cause
    • Splenic or portal vein thrombosis (prehepatic)
  • Results/complication
    • Development of venous collaterals
      • Esophageal varices (hematemesis in alcoholics)
        • Dilated tortuors veins in Lower esophagus) = first sign of cirrhosis and portal hypertension
      • Hemorrhoids
      • Enlarged veins on anterior abdominal wall
      • Spider angiomas
    • Ascites (fluid in abdominal cavity)
      • LIVER DISEASE = MOST COMMON CAUSE
    • Splenomegaly (congestive)
84
Q

What is the following in relation to the liver:

  • Kernicterus
  • Hepatitis (with relation to liver)
  • Transaminitis
  • Viral hepatitis
A
  • Kernicterus
    • newborn infants with high levels of bilirubin that accumulates in the brain (form of crippling)
  • Hepatitis (with relation to liver)
    • Inflammation of the liver
  • Transaminitis
    • Damage to liver cells -> release enzymes into blood -> increase serum levels of enzymes (transaminases = AST = aspertate, ALT = alanine)
    • Increase transaminases used to diagnose liver disease
  • Viral hepatitis
    • Liver inflammation caused by a virus
85
Q

Nephroliniasis

A

Nephroliniasis (Kidney stones)

  • Forms in renal pelvis, calyces and passes into urinary system
  • More often in M>F; rare in children
  • Predisposing factors
    • Dehydration, infection, changes in urine pH, obstruction of urine flow, immobilization with bone reabsorption, Metabolic factors (hyperparathyroidism with hypercalcemia), renal acidosis, increased uric acid, defective oxalate metabolism
  • Stone composition
    • Calcium oxalate or calcium phosphate (most common)
      • ​​Calcium stones account for 80-90% of urinary stones. They are composed of calcium, oxalate, calcium phosphate, or both
    • Struvite (from infection)
    • Uric acid (from metabolic disorders, obesity)
    • Cystine (inborn errors of metabolism)
  • Clinical symptoms:
    • Usually asymptomatic (until stone passes)
    • Renal colic (sever pain) - once stone is in ureter
  • Complications
    • obstruction of ureter (presure and pain)
    • Pyelonephritis (acute or chronic)
    • Hydronephrosis (urine cannot get out)
86
Q

What is Hydronephrosis

A

Hydronephrosis

  • Abnormal dilation of renal pelvis and calyces of one or both kidneys
  • Caused by urinary track obstruction (Stone!!)
    • Decreased urine flow
    • Increased pressure behind the obstruction
    • Renal pelvis and calyces dilate
  • Physical manifestion
    • NOT a disease process itself
    • Disease = stone, stricture (restrict activity), benign prostatic hyperplasia, etc
87
Q

What is Pyelonephritis?

A

Pyelonephritis

  • Infection of the renal pelvis (kidney and ureter), usually E. coli
  • Cause:
    • Most often from a urinary tract infection (UTI)
    • Retrograde/backflow bacteria-laden urine from bladder into ureter up to kidney pelvis (vesicoureteral reflex) = from LUT
  • Forms:
    • Acute
      • Active infection of the renal pelvis
      • Abscess can develop; renal pelvis fills with pus (neutrophil rich)
    • Chronic
      • Scarring fibrosis; renal failure is possible
88
Q

What is the following and what is it caused by:

  • Hematuria
  • Glucosuria
  • Ketonuria
  • Proteinuria
A
  • Hematuria
    • blood in urine (Women = in urine; Men = bloody ejaculation from prostate; Children = bleeding disorder, recent strep infection may imply post-strep GMN)
      • Poststreptococcal GMN is the classic cause of blood in urine in children
    • Kidney or urinary tract disease
  • Glucosuria
    • Glucose in urine
    • Diabetes mellitus
  • Ketonuria
    • Ketone in urine; acetonelike odor
    • Starvation, uncontrolled Dibetes mellitus, Alcohol intoxicaation
  • Proteinuria
    • Protein in urine
    • Kidney disease
89
Q

What is Polycystic Kidney Disease (PCKD)

A

Polycystic Kidney Disease (PCKD)

  • Adult form (APCKD) = Autosomal dominant
  • Inherited disorder with multiple cysts on the kidney
  • Caused by mutation in the PKD gene
  • Course
    • Early stages
      • Kidney enlargement (as cysts form and grow)
      • Kidney function altered, resulting in:
        • Chronic high blood pressure; hypertension caused by polycystic kidneys is difficult to control
        • Anemia
        • Erythrocytosis; if cysts cause increased erythropoietin (increases RBC)
        • Kidney infection
        • Flank pain, if bleeding into a cyst also
    • Later
      • Slow progressive
      • Ultimately resulting in end stage kidney failure (and liver cysts)
    • APCKD also associated with liver disesae and infection of liver cysts
  • Childhood form
    • Autosomal recessive form of polycystic kidney disease
    • More serious form appears in infancy or childhood
    • Course:
      • Progressive rapidly
      • Resulting in ESRD (end stage renal disease)
        • Kidney failure leads to death in infancy or childhood
  • NOTE: kidney stones are less common in PCKD
90
Q

What is kidney disease often associated with?

A

Kidney disease is often associated with malignant hypertension. Malignant hypertension is defined as BP over 200/140 and can cause papilledema and CNS dysfunction

91
Q

Explain Nephrosclerosis

A

Nephrosclerosis

  • Renal impairment secondary to artherosclerosis or hypertension
  • Arterial nephrosclerosis
    • ​​Atrophy and scarring of the kidney
    • Due to artheriosclerotic thickening of the walls of large branches of renal arteries
  • Arteriolar nephrosclerosis
    • Arterioles thicken
    • Areas they supply undergo ischemic atrophy and interstitial fibrosis
    • Associated with Hypertension
  • Malignant nephrosclerosis
    • Inflammation of renal arterioles
    • Results in rapid deterioration of renal function
    • Accompanies malignant hypertension
92
Q

What is Nephrotic Syndrome

A

Nephrotic Syndrome

  • Not a disease itself
    • Glomerular defect underlies the process, indicating renal damage
    • Can affect anyone at any age
  • Characterized by:
    • Proteinuria (LOTS OF PROTEIN IN THE URINE)
    • Hypoalbuminemia
    • Hyperlipidemia - Fat = edema
      • ​​Secondary to increased hepatic fat synthesis and decreased fat catabolism
    • Edema (increased salt and water retention)
  • Cause: increased glomerular capillary permeability
    • Leads to decrease blood protein (albumin)
    • Leads to increased protein in urine
  • Associated diseases:
    • Malignancy such as leukemia, lymphoma and multiple myeloma
    • Autoimmune disease such as lupus, Goodpasture’s syndrome and Sjogren’s syndrome
    • Infections such as bacterial and HIV
    • Diabetes mellitus
    • NSAIDS
  • Clinical symptoms
    • Loss of appetite, malaise (sick feelign), puffy eyelids, abdominal pain, muscle wasting, tissue swelling/edema, Frothy urine (protein-laden)

Primary NS = limited to kidneys only

Secondary NS = disease affets the kidneys and other organs

(NOTE: Lipiduria: cholesterol, triglycerides, lipoprotiens leak into the urine)

93
Q

What are Glomerularnephropathies?

A

Glomerularnephropathies

  • Kidney disorders where inflammation affects mainly the glomeruli
  • Varied causes, but glomeruli respond to injury similarly
  • Acute nephritic syndrome
    • Ex. Acute post-streptococcal glomerulonephritis
      • most common in boys 3-7. Starts suddenly and resolves quickly
    • Acute glomerular inflammation
    • Sudden hematuria (clumps of RBCs (casts))
    • Protein in urine
  • Rapidly progressive nephritic syndrome
    • Ex: RPGN
      • Uncommon disorder; usually occurs 50-60
      • Starts suddenly and worsens rapidly
      • Most of the gomeruli are partialy destroyed = Kidney failure -> Idiopathic or associated with proliferative glomerular disease (Acute GN)
  • Nephrotic Syndrome
    • Finding:
      • Proteinuria (LOTS!!!!!)
      • Hypoalbuminemia
      • Generalized edema
      • Hyperlipidemia
      • Hypercholesterolemia
  • Chronic Nephritis Syndrome (AKA chronic glomerulonephritis)
    • Examples:
      • SLE
      • Goodpasture’s syndrome
      • Acute GN
      • Slowly progressive disease
      • Inflammation of the glomeruli
        • Sclerosis
        • Scarring
        • Eventual renal failure

NBDE Part 1 (7 decks)

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