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
What is the difference between hamartoma and choristoma?
**_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
26
Explain Edema and how it is caused
***_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
27
Name and describe the two types of Edema
***_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**)
28
Name and describe examples of Transudate
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)
29
What does Right-sided conjestive heart failure lead to vs. Left-sided conjestive heart failure?
* **_Right-sided conjestive heart failure_** * results in peripheral edema * **_Left-sided conjestive heart failure_** * results in pulmonary edema
30
What are examples of Edemas and causes
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
31
What is Shock
**_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
32
What are the Major categories of shock and describe
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)
33
Name and decribe the three stages of shock
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)
34
Describe Congestion (Hyperemia) and its types
**_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)
35
What is Thrombosis What is the difference between Arterial and Venous Thrombi
***_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
36
What is the Virchow's Triad for Thrombosis
Virchow's Triad for Thrombosis * Endothelial injury * Alteration in blood flow * Hypercoagulability of blood
37
What are the Lines of Zahn for Arterial thrombi?
***_Lines of Zahn (arterial thrombi)_*** * **White** (fibrin and platelet) layers **alternating** with **dark** (RBC) layers * Indicated **_thrombosis in aorta or heart_** before death
38
That are the types of Thrombus - Name and describe
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
What are the predisposing factors to thrombosis Both Atrial and Venous thrombosis
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
What are Embolus
***_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
Pulmonary Embolism
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
Explain Artheriosclerosis and Atherosclerosis
**_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
What is Familial hypercholesterolemia?
Familial hypercholesterolemia * Autosomal dominant diseae * Anomalies of LDL (low-density lipoprotein) receptors * Atherosclerosis and its complications * Xanthomas * MI by age 20
44
What are the two types of Hypertension and explain
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
What is an Aortic Aneurysm and Aortic Dissection
***_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
Explain The types of Infections of the heart
Infections of the heart * **_Pericardium_** * pericarditis * **_Myocardium_** * myocarditis, often viral * **_Endocardium and heart valves_** * Endocarditis, often bacterial or inflammatory
47
What is Endocarditis
***_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
What are the three types of Endocarditis?
**_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
What is Coronary artery disease (CAD)?
***_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
What is Angina and explain the types
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
What is a Myocardial infarction and what are the types
**_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
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Where is Creatine phosphokinase (CPK) enzyme found in?
CPK: Enzyme found in (increases when damage to): Heart Brain Skeletal muscle **NOT** found in the liver....
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What is heart failure
**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)
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Explain Cardiovascular Pulmonary Cross-correlation of Carbon monoxide (CO) poisoning and Pulmonary Edema
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_**)
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What is Angina Pectoris?
**_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
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Mechanisms of Asthma Precipitation
* **_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)
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What is Chronic Obstructive Pulmonary Disease (COPD) and what are the two categories
***_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
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Explain Emphysema and state the types
**_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
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What are restrictive lung diseases signs/lung affect
***_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)
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What are the mechanisms of airway obstruction
***_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)**
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Explain Chronic Bronchitis (COPD)
***_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
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What are the following: * Atelectasis * Anthracosis * Silicosis * Asbestos
* **_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
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What is Sarcoidosis?
**_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
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What is Mesothelioma
Rare tumor involves parietal or visceral pleura Associated with asbestos exposure: 25-45 year latency Diffuse lesion; spreads over lung surface
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Explain Pneumonia
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
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Name the types of Pneumonia Causes, Findings, Age What is the difference between Viral and Bacterial Pneumonia?
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
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What is a lung abscess and what is the most common predisposing factor?
**_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
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What is Hemoptysis and when does it occur
**_Hemoptysis_** Coughing up **blood** (or blood-streaked sputum) * Respiratory infections (minor URIs) * Bronchitis * TB * Pneumonia * Bronchogenic carcinoma * Idiopathic pulmonary hemosiderosis (iron in lungs)
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What is Tuberculosis (TB)?
**_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
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Name the three types of Tuberculosis (TB), what sites they are found and characteristics
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
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What is Ghon's complex?
Ghon's complex = calcified primary lesion + lymph node involvement Seen in Primary TB and reactivated in Secondary TB
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What is Mallory-Weiss Syndrome?
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
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What is the following: * Achalsia * Hiatal hernia * Gastroesophageal Reflex Disease (GERD) * Esophageal Ulcers What is the Zollinger-Ellison triad?
* **_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
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What is Peptic Ulcer Disease (PUD)
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
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Hematemesis
***_Hematemesis_*** * Vomiting of bright red blood, indicating rapid upper GI tract bleeding * Assoicated with **esophageal varices** (common in *_alcoholics_*) or **peptic ulcers**
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What are the following that are associated with Small and Large Intestines * Meckel Diverticulum * Intestinal Lymphangiectasia
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
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What are the following that are associated with Small and Large Intestines **Inflammatory Bowl Disease** (describe breakdown of the two types)
**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**
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Explain Malabsorption syndromes and state the types and what the do
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
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Explain Pancreatitis
***_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
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Explain Cholelithiasis
***_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
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Explain Cholesterolosis and Gallbladder Diverticulosis
**_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
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What is Cirrhosis (of liver) Characteristics Cause Clinical findings/complications
***_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)
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What is Portal Hypertension Characteristics Cause Clinical findings/complications
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)
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What is the following in relation to the liver: * Kernicterus * Hepatitis (with relation to liver) * Transaminitis * Viral hepatitis
* **_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
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Nephroliniasis
***_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)
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What is Hydronephrosis
***_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
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What is Pyelonephritis?
***_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
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What is the following and what is it caused by: * Hematuria * Glucosuria * Ketonuria * Proteinuria
* ***_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
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What is Polycystic Kidney Disease (PCKD)
***_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
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What is kidney disease often associated with?
Kidney disease is often associated with malignant hypertension. Malignant hypertension is defined as BP over 200/140 and can cause papilledema and CNS dysfunction
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Explain Nephrosclerosis
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
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What is Nephrotic Syndrome
Nephr***_o_***tic Syndrome * Not a disease itself * Glomerular defect underlies the process, indicating renal damage * Can affect anyone at any age * Characterized by: * *_Pr**o**teinuria (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)
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What are Glomerularnephropathies?
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
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