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Pathophysiology Final Study Guide
Patho Section 1
Cell & Tissue Function/Dysfunction

​Atrophy: decrease in size of cells
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​Hyperplasia: increase in number of cells
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​Dysplasia: cells vary in size & shape within a tissue
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​Neoplasm: tumor
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​Hypoxia: reduced oxygen in tissue
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​Temperature: inactivation of some enzymes, damages organelles, protein c​ oagulation,
disruption of cell membrane
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​Nutritional Deficits
Cell Death
​Apoptosis:programmed cell death controlled by genetics
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​Liquification:dead cells liquefy due to release of enzymes
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​Caseous:form of coagulation necrosis, thick, yellowish, cheesy
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Tissue Damage from Chemicals

​Exogenous: from environment
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​Hyperthermia: causes general vasodilatation, decrease in circulating blood
​volume
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​allergic reaction to insect proteins
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​Fluids: may contain enzymes or chemicals:saliva, tears, gastric, sweat
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​Inflammation: automatic response to cell injury
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​Macrophages: monocytes that enter tissue & act as phagocytes
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​White Blood Cells
​Granulocytes
​Neutrophils: work by phagocytosis
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​Eosinophils:combat the effects of histamine
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​Lymphocytes: B & T
Acute Inflammation

​Vascular Response: vasodilatation & increased capillary permeability
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m
Exudate

​Serous: watery, mostly fluids, some proteins and WBC’s
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​Purulent: thick, yellow-green, contains leukocytes, cell debris & microorganisms
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Local Effects of Inflammation-Cardinal Signs of Inflammation
​Redness & Warmth: due to increased blood flow to area
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​Pain: pressure on free nerve endings, chemical mediators irritate nerves
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Systemic Effects of Inflammation
​Mild Fever: due to resetting of hypothalamic thermoregulatory set point, release

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​Malaise
​Fatigue
​Headache
​Anorexia

​

Treatment of Inflammation: drugs may decrease capillary permeability, reduce number of

​leukocytes & mast cells
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​Regeneration: damaged tissue is replaced by identical tissue
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​1st Intention: wound is clean, edges are close together with minimal gap
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​Scar Formation: fibroblasts proliferate, abnormal amount of collagen
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​Ulceration: blood supply around scar is impaired resulting in tissue
​breakdown
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Partial thickness ulcer-red or pink ie
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​2
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​3
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​4
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Drainage
​Transudate: clear & watery
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Contains serum/blood thin & watery
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Contains proteins & WBC’s Thick
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Contains leukocytes and necrotic debris, thick
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Contains pathogens, thick
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​Wet Gangrene: tissue necrosis + bacterial infection
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​Black Gangrene: gangrenous borders, mummified skin
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​ 9-1 m
​ in sx in LE

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9 c​ laudication pain(leg pain w/ walking)

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5 i​ schemic rest pain
​
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LE Elevation to 60º for 1 minute
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​2
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>30seconds
​means arterial insufficiency
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Immune Response-Third Body Defense

​Humeral Immunity: antibodies are produced to protect body & stored in blood
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​Antigens:immunogens, proteins, polysaccharides, glycoproteins on cell surface
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​Lymphocytes:primary cell in immune response,
​T: has 3 subgroups made in bone marrow & differentiate in
t​ hymus, cell mediated i​ mmunity, can target certain cells
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Cytotoxic T:cells destroy cells bind to antigen & release enzymes
​2
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Memory T: remember antigens
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​Natural Killer:kill tumor or virus infected cells w/o prior exposure
​Antibodies
​IgG:most common, can activate compliment, cross placenta, primary &
​secondary immune response
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​IgM:can activate compliment, natural antibodies ie
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​IgE
​IgD
​Compliment System:antigen-antibody complex, activated during immune rxn w/
​IgG or IgM
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​Immune Response
​Primary: 1 exposure to antigen, 1-2 weeks needed for effective antibodies
​Secondary:repeat exposure to same antigen, effective response in 1-3 days
I​ mmunity: Innate-always present
...

st

Hypersensitivity Reactions

​Type 1 Hypersensitivity:allergic rxn, exposed to allergen causes development of
IgE’s,activate mast cells and causes inflammation
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Hay fever, allergies, asthma

​

​Type 2 Hypersensitivity:cytotoxic hypersensitivity
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Ie
i​ ncompatible
blood type exposure
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​Type 4:Cell Mediated or delayed response by T-lymphocytes
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Ie
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Immune System Malfunction

​Hypersensitivity: full system immune response to non-noxious stimulus
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​Interventions/Treatment:avoid triggers, medicate
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​Autoimmune
​Multiple Sclerosis: autoimmune demyelinization of nerves in brain &CNS
​Classification
​Clinically Isolated Syndrome-only suffer 1 attack
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​Tests & Measures: MRI, visual evoked potentials, CSF analysis
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​Myasthenia Gravis: antibodies destroy Ach receptors at NM junction
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​Fibromyalgia: generalized musculoskeletal pain > 3 months, multiple
​tender points affecting all 4 quadrants, 11/18 points, 4Kg force painful
​Rheumatiod Arthritis:autoimmune destruction of joints affects multiple

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​Scleroderma:affects microvessels causing hypoxia in all tissue
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Skin &

​Sjogren’s Syndrome: autoimmune disease » loss of fluid for tears/saliva
​Hashimoto’s Disease: autoimmune thyroid disease, causes hypothyroidism
​Graves Disease: hyperthyroidism,
​Type 1 Diabetes: autoimmune destruction of pancreas cells » no insulin
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​Ulcerative Colitis: ulcers in lower intestines, may begin in rectum
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​Toxoplasmosis: parasitic infection
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​Histoplasmosis: fungal infection diagnoses based on organ involved
st

Micro-organisms

​Bacteria-unicellular organisms, no nucleus, divide by binary fission
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​Spirochetes-syphillis, cholerae
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​Gram Negative: retains crystal violet, no outer layer, thick peptidoglycan layer
​Toxins
​Exotoxins: produced by gram+ bacteria
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Released when bacteria die causing shock
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New viruses made in
​cytoplasm & released by lysis or budding from host cell
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Ie
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​Fungi: eukaryotic organisms, primarily affect skin or mucous membranes
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Ie
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Mad Cow
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​Aerosol
​Vector
Nosocomial Infections: infections that occur in healthcare setting
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​Acute Infection: fully developed infectious disease with peak clinical signs
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​Subclinical Infection: Microbe can reproduce in body but no signs present
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Complimentary Medicine
​Red Flags: refer to Dr
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Screening Lab

​Fingernails
​Absent Lunula: anemia, malnutrition
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​Red Luluna: cardiovascular disease, collagen disease of vessels, blood CA
​Mee’s Lines: metal toxicity, chemotherapy exposure
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​Splinter Hemorrhages bacterial endocarditis, lupus, renal failure, psoriasis
​Terry’s Nails:half& half appearance:edema & anemia »renal/liver disease
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​-Hematuria 1
​

Breast Cancer:

Cervix cancer:

​

Colorectal cancer:

st

sign with changes in urination

​-New lump is most common symptom
​-Manual palpation better catch than mammogram
​-often asymptomatic
​-vaginal discharge, abnormal bleeding, pain during intercourse
​-change in bowel habits most common
​-Diarrhea, constipation, more narrow stools, blood in stool
​-Bright blood-lower GI, Dark/black blood-Upper GI

Lung cancer:

​-persistent cough with or w/o chest pain
​-Feeling of an infection that just won’t go away

Prostate cancer:

​-weak interrupted urine flow, frequent urination esp
...
w/ injury

Skin Cancer:

​-Any new growth on skin should be examined
​-Spot or bump that changes size, irregular borders
​-Sore that will not heal

Change in bowel/other habits
A sore that does not heal
Unusual bleeding or discharge
Thickening or lump in breast
Indigestion or difficulty swallowing, unexplained weight loss
Obvious change in wart or mole
Nagging cough/hoarseness
Fluid/Electrolyte imbalance
Water

​-60% adult body wt, 70% infants, higher % in females

Fluid compartments

​-Intracellular 2/3 water in body

-ECF 1/3

​*Interstitial 3/4, Intravascular 1/4, Cerebro Spinal Fluid 1%
Control Fluid Balance->Thirst mechanism
-Antidiuretic Hormone (ADH): fluid output
-Aldosterone: Reabsorption of water and sodium
-Atrial Natriuretic Peptide (ANP): lowers BP by controlling blood volume
EDEMA: fluid excess in interstitial compartment
DEHYDRATION: Signs-decreased skin turgor, sunken eyes, low BP, rapid weak pulse, high temp

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Insulin forces K+ into cell
Tract motility
Renal failure, deficit aldosterone,
Cardiac dysrythmias, mm weakness
leakage of K+ from ICF into ECF,
common progressing to paralysis,
prolonged acidosis (H+ replaces)
respiratory arrest
Hypothyroidism, malabsorption
Increased permeability/ --excitability
syndrome, deficient serum albumin, of nerve membranes,spont stim of
increased serum pH
skeletal mm, Tetany, weak Heart
contractions
Uncontrolled release from bones Depressed neuromm activity
demineralization from immobil
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PROTUDING TONGUES
odd bouts of Laughter, Balance
disorders
Missing part chromosome 5, mutation Hi “CAT-like” cry, webbed toes &
at
fingers, DOWNward slant to wide set
eyes, skin tags ant
...
effects nervous syst and skin,
birthmarks called café-au-lait,
Autosomal dominant,
freckles in armpits and groin,
purplish RUBBERY lesions on skin
X-linked, lose “bit” of chromosome

CAUSE(S)
Chromosome XV

CHARACTERISTICS
Extreme hunger/overeating, obsessed
w FOOD, temper tantrums, violent
outbursts, @ 1 Y
...
become
ravenously hungry
Broad nasal bridge, PROTRUDING

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4
Cystic Fibrosis
Single point mutation CFTR

Muscular Dystrophy

Dystrophin-over 30 different genetic
diseases

jaw, ear anomalies, SPEECH &
middle ear problems, SLEEP
disturbances
Sudden Mood changes
Teenagers less developed,
prepubescent testosterone helps,
testosterone levels to diagnose,
infertility
WEBBED neck!! Underdeveloped
BREASTS
High BP, Type II diabetes
Girls TALL, often not diagnosed, no
long term problems
50% retardation, PUFFINESS around
eyes, long neck, sloping shoulders,
Poor DEPTH perception
Life limiting (30s), frequent coughing
w/ thick sputum, salty-skin, frequent
lung infections,
-Duschenne most common (missing
dystrophin), affects skeletal & cardiac
Muscle
-Fascioscapulohumeral-faulty
dystrophin
-Myotonic; congenital, juvenile, adult,
late onset-over 50

ACID-BASE Imbalance -> Normal 7
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35 to 7
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o Artificial EPO (stimulates RBC production)
o Bone marrow Transplants: some cancers, immune deficiencies, blood cell disease
ANEMIAS- can lead to ANGINA or CHF
▪ Hemoglobin deficit= reduction in oxygen transport
▪ General signs
• Fatigue, pale face, dyspnea, tachycardia
▪ Causes
• Nutrient deficiency
• Impaired bone marrow
• Blood loss or excessive destruction of RBCs
Iron deficiency: impairs hemoglobin, very common, usually underlying CAUSE
Pernicious Anemia
o Large, immature, nucleated erythrocytes(RBCs)
o SYMPTOMS-> Tongue large, RED, sore, shiny

o
• Aplastic Anemia
o Temporary or permanent impairment or failure of bone marrow
o Bone marrow cells replaced by FAT
o Cause must be ID’d for prompt treatment & marrow recover or is LIFE threatening
• Hemolytic anemia
o CAUSE: excessive destruction of RBCs via many causes

• Sickle Cell Anemia-> abnormal hemoglobin
o Genetic condition; autosomal rec
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• Polycythemia
o Primary polycythemia->Increased rate of RBC production
▪ Secondary polycythemia-> Increased RBC production due to prolonged Hypoxia
o Concerns for both:
▪ Sluggish blood flow
▪ Increased BP & hypertrophied heart
• Indications of Blood clotting Disorders
o Persistent bleeding in gums & nose bleeds, bleeding into joint, coughing up/vomiting blood, blood
in feces, vomiting, low BP

• Causes of clotting disorders
o Defective platelet function
o Long term use of warfarin
• Hemophilia A (classic)
o Most common inherited clotting disorder

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May also be in front of trunk
Location
frequently in abdomen over affected
organ
Associated signs & symptoms Jaundice, skin rash, weight loss,
fatigue, low-grade fever, muscular
weakness, frequent infections

Musculoskeletal
Sudden (gradual when related to
overuse)
Decrease with Rest

Increase with use affected region
SHARP
Depends on if acute, subacute, or
chronic
Located over injury sight
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Patho 3
Cardiovascular Disorders - Gould Ch
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g
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’s)
​-Beta-blockers – prevent CNS stimulation of heart
​-Ca2+ channel blockers – decrease contractility of heart
- anti-hypertensives – ACE inhibitors (angiotensin converting enzyme – work via renal
system), diuretics, cholesterol decreasing drugs, anticoagulates to prevent clots
Arteriosclerosis – hardening, narrowing of arteries – fibrous tissue formation (tunica adventicia
grows) à constriction

​-caused by hypertension
Atherosclerosis – plaque buildup in arteries, “atheromas”
​-coronary occlusion àangina, MI
​-clot to brain àTIA or stroke
​-clot in periphery à can lead to aneurysm
Cholesterol

​-HDL – mostly protein, little fat – carries lipids to liver for excretion
​-LDL – mostly fat, little protein – carries lipids to cells of body
​-largely responsible for atheroma formation
Risk factors for cardiovasc problems – age, heredity, obesity, sedentary lifestyle, smoking,
glycemic control, serum lipids
Angina Pectoris – O2 low in heart muscle à severe, crushing chest pain, “angere”= “to choke”
Myocardial infarction – cell death from O2 deprivation à replaced with fibrous tissue

​-majority occur in left ventricle
Congestive Heart Failure
​-Forward effect – Not enough blood going out, pump FAILURE
​-Backward effect – CONGESTION of blood behind failing ventricle
​-One side fails first, ultimately leads to failure of other side
-Decreased CO (cardiac output) one side àcompensation mechanisms –
vasoconstriction, water & sodium retention, increased blood volume àincreased
work for the heart
-Eventually muscles of affected side weaken àcongestion behind affected side à
unaffected side pumps against increased resistance à Previously unaffected side
weakens

​Right side failure – systemic congestion
​Left side failure – pulmonary congestion
-pericarditis à effusion à fibrous adhesions
-myocarditis à arrhythmias
-endocarditis à infection of heart valves àcan lead to fibrosis

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-epinephrine in blood stream = inhibitory for endothelial cells, excitatory for
smooth muscle underneath à vasoconstriction and incr
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BP
Aneurysms

​-fusiform – bulge in all directions
​-saccular – sac forms on one side – pooling of blood causing clotting àthrombus formed
-dissecting – most dangerous – blood runs between tunica intima and media – dissecting
aortic aneurysm =ticking time bomb
Circulatory shock – severe hypotension

​-causes = hypovolemic, cardiogenic, septic, distributive (vasogenic, neurogenic,
anaphylactic)
-compensations – SNS incr
...

Venous insufficiency

​-valves fail due to age, injury, sendentary life, obesity
​-chronic pooling of blood in LE
​-brown, blue, purple skin in feet and toes – waste accumulation!
​-minor trauma à large wound! Hard to treat
Lymphomas – cancer of T-cells and B-cells

​-Hodgkins – Tcell; Non-Hodgkins- B-cell
​-large lymph nodes and spleen
​-good prognosis if tx’d before metastasis
Respiratory Disorders – Gould Ch
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​-air goes out
​-Sympathetic activation à smooth mm relaxation, bronchodilation
​-alveoli = squamous epithelium – maximizes gas exchange
​-covered with surfactant – reduce surface tension of fluid, prevent collapse
​-macrophages!
​-intrapleural pressure a shade under atmospheric pressure
​-feeling when you hold breath due to chemoreceptors for CO2
...
CO2 – compensate with hypoventilation
Hyper/hypoxemia – O2 sats

​-As more O2 binds to hemoglobin, affinity for O2 rises – aids in acquisition and release
of O2
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​-grown more resistant to drugs in recent years
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​-inflammation of mucosa à bronchoconstriction, obstructive mucus
​-can cause atelectasis –collapse of lung because of airway blockage
(-pneumothorax involves a collapsed lung caused by mechanical damage or a
rupture of a small airsac or “bleb” on outside of lung)
-presents with hypoxia, respiratory alkalosis (initially due to hyperventilation), cyanosis,
cough, tightness in chest, thick mucus, tachycardia
-treat with inhalers and glucocorticoids
COPDs –progressive degeneration
​
-Emphysema –“pink puffers” – red face, overinflation

​-destruction of alveolar walls àpermanent inflation
-smoking eliminates anti-trypsin that inhibits enzyme that destroys elastin àelastin of
alveoli destroyedàloss of septae between alveolar sacs àdecreased surface area for gas
exchange
-presents with “barrel chest” – ribs fixed in inspiration position
-Chronic Bronchitis – “blue bloater”

​-inflammatory obstruction àrepeat infections, progressive, irreversible damage of
bronchioles
​-hypertrophy, hyperplasia of mucus glands, fibrosis
​-Present with constant cough, SOB, cyanosis
​-treat by Stopping Smoking, O2 supplementation, available vaccinations for at risk
infections
Emphysema
Chronic Bronchitis
Alveoli affected
Bronchioles affected
Septae walls destroyed Increased secretions
Some cough
Lots of coughing
Little sputum
Lots of sputum
No cyanosis
Cyanosis
Some infections
Frequent infections
-Bronchiectasis

​-permanent dilation of medium-to-large-sized bronchi
​-caused by recurrent inflammation
Restrictive Pulmonary Disorders – impaired lung expansion
​-often abnormal chest wall or lung inself
-Pneumoconiosis
​-exposure to irritants – coal workers
​-inflammationàfibrosis, “stiff lung”
​- insidious onset
-Vascular Disorders
​-Fluid collects in alveoli and interstitial fluid
​-lung expansion decr, O2 in blood decr,
​-leads to pulmonary hypertension and edema
-Pulmonary embolism
​-blood clot from veins pumped to lungs – deadly
-Atelectasis

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Stomach

​Gastrin cells (G cells): initiated by food entering stomach, stimulates chief and parietal cells
​Intrinsic factor (parietal cells): needed for absorption of vitamin B12
​HCL (parietal cells): activates pepsinogen, creates optimal pH ~2, denatures proteins
​Pepsinogen (chief cells): pepsin not activated until pH of 6

​

Liver “Metabolic factory of the body”

​1)Storage of nutrients 2) Maintains blood glucose 3) Blood reservoir 4) Produces bile, plasma proteins,
​blood clotting factors, cholesterol/lipoproteins 5) Metabolic processes (detoxification, conversions)
​Glucose -> Glycogen = Glycogenesis (when glycogen supply low)
​Protein, Fat -> Glycogen = Glyconeogenesis
​Glycogen -> Glucose = Glycogenolysis (maintains blood glucose levels)
Pancreas

​Exocrine (secreting digestive enzymes and electrolytes) and endocrine organ
​Trypsin, chymotrypsin, carboxypeptidase-break proteins
​Ribonuclease-break nucleic acids
​Pancreatic amylase-break starch
​Lipase-break lipids
GI tract

​Ileum=major site of nutrient absorption, villi (folds of mucosa)
​Large intestine=fluid and electrolyte reabsorption, movement slow to allow absorption of water, vitamin K
​synthesis (essential for blood clotting)
Neural and hormonal control

​PNS (vagus mainly): increased motility and secretions, SNS: inhibits GI activity
​Gastrin: increases gastric motility and promotes stomach entering, Secretin: decreases gastric secretions,
​Cholecystokinin: inhibits gastric emptying
​
Upper GI Tract Disorders (includes differential diagnosis)

Disorder
Dysphagia

Description
Difficulty swallowing

Causes

1) Neurological deficit

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pylori infection
(gastric and
Common in proximal duodenum and
1) Increased acid-pepsin secretions
duodenal)
antrum of stomach (ulcers in general
2) Inadequate blood supply
rarely found in large intestine)
3) Excessive glucocorticoid secretion
4) Ulcerogenic subtances
Stress Ulcers
Rapid onset, may form within hours of
Severe trauma: Burns (curling’s
precipitating event
ulcers), head injury (cushing’s ulcers)
Systemic: hemorrage, sepsis
(ischemic ulcers)
Gastric Cancer
Primarily in mucous glands and in
Gone down bc we have preservatives
antrum or pyloric area, poor prognosis
w/ food
Pyloric Stenosis Narrowing and obstruction of pyloric
May be developmental anomaly or
sphinctor
acquired later in life

Liver and Pancreas Disorders (includes differential diagnosis)
Gallbladder Disorders
Description
Cholelithiasis
Formation of gallstones*
Cholecystitis
Inflammation of gallbladder and cystic
duct
Cholangitis
Inflammation related to infection of bile
ducts
Choledocholithiasis
Obstruction of biliary tract by gallstones
(due to larger stones)

*Risk factors for developing gallstones: Women (2x more likely), high cholesterol, obesity, multi parity (several
children), use of oral contraceptives or estrogen supplements, hemolytic anemia, alcoholic cirrhosis
Disorder
Description
Jaundice Yellowish color of skin (not disease itself but sign of
other disorders)
Prehapatic: unconjugated bilirubin elevated
Intrahepatic: unconjugated and conjugated bilirubin
elevated
Posthepatic: conjugated bilirubin elevated
Hepatitis
Inflammation of liver
Mild: impaired hepatocyte function
Severe: necrosis and obstruction of blood/bile flow
along w/ impaired hepatocyte function
Cirrhosis
Progressive destruction of liver
Stage 1=fatty liver (asymptomatic & reversible)

Causes
Prehepatic: excessive destruction
of RBCs
Intrahepatic: disease or damage to
hepatocytes
Posthepatic: obstruction of bile
flow into gallbladder or duodenum

1) Idiopathic (fatty liver)
2) Infection (viral or non-viral)*
1) alcohol (most common)
2) biliary: obstruction of bile flow

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nausea, fever, elevated WBC, do NOT
see blood in stool
Early diagnosis essential
Symptoms=alternating diarrhea and
constipation, bleeding,weight loss,
anemia, fatigue, red blood in stool, pain
doesn’t often occur
Most diagnosed cancer next to skin
cancer

Colorectal Cancer

Most from adenomatous polyps
(polyp does not always mean
cancer!)
Risk factors: familial multiple
polyps, long-term ulcerative
colitis, diet low in fiber (why
susceptibility has increased)

Intestinal Obstruction Lack of movement of intestinal contents Mechanical obstruc
...

-impairment of peristalsis
-Ex: spinal cord injury
Peritonitis
Inflammation of peritoneal membranes 1) Chemical peritonitis: caused by
Symptoms: sudden severe and
foreign chemical in peritoneal
generalized abdominal pain, abdominal (bile, chyme, etc)
distention, dehydration, low blood
2) Bacterial peritonitis: direct
pressure,tachycardia, vomiting
trauma affecting intestines,
ruptured appendix
1) Abdominal surgery (infection
may develop)
2) Pelvic inflammatory disease in
women

1) Change in bowel motility that is

Irritable Bowel
Syndrome

associated with pain

2) Must be there 12 weeks out of the
year

3) Do NOT see blood in stool

Urinary Disorders
Urinary System Overview
Kidney

​Nephron=functional unit of the kidney (>1 million), consists of renal corpuscle (filtration unit) and renal
​tubule
​ADH-prevents water loss (increases reabsorption of water in distal convoluted tubules and collect
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​

(Renin secreted in response to reduced afferent arteriole blood flow)

Urinalysis
Cloudy-presence of large amounts of protein, blood, bacteria, and pus

​

Blood: if large amount=increased glomerular permeability or hemorrhage, if small amount=infection,
inflammation or tumors in urinary tract
Dark color-hematuria, excessive bilirubin, highly concentrated urine
Unusual smell or odor-infection, diet, or medication
Elevated BUN and creatine=failure to excrete nitrogen waste
Metabolic acidosis (low pH, low bicarbonate)=failure of tubules to control acid/base balance

Urinary System Disorders (includes differential diagnosis)
Disorder
Urinary Tract Infection

Glomerulonephritis

Nephrotic Syndrome

Bladder cancer

Vascular Disorders

Adult Polycystic kidney
disease
Polycystic disease in
children
Acute Renal Failure

Chronic Renal Failure

Description
Lower=cystitis and urethritis
(hyperactive bladder and reduced
capacity), may have systemic signs w/
painful urination
Upper=pyelonephritis (in one or both
kidneys: purulent exudate and abscess
block blood and urine flow), systemic
sign of high fever *can lead to renal
failure*
Decreased GFR rate (decreased urine
output, elevated blood pressure and
edema)
Metabolic acidosis
Bloody, foamy urine and pain
Increased permeability in glomerular
capillaries
Hypoalbuminemia,increased
aldosetrone, severe edema
Often develops as multiple tumors
Early signs:hematuria and dysuria

Thickening/hardening of walls and
small arteries
Reduces blood to kidney-stimulation of
renin (increases blood pressure)
Manifests around 40
Multiple cysts in both kidneys-leads to
chronic renal failure
Manifested at birth, child dies in first
month or is stillborn
Rapid onset
Metabolic acidosis and hyperkalemia
Ogliuria, increased serum urea

Gradual, irreversible destruction of
kidneys (<10%=end stage)
Asymptomatic w/ up to 40% left
Symptoms later on=polyuria with dilute
urine, anemia, fatigue
Axotemia=renal insufficiency<25%

Cause
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Kidney Stones

Wilms Tumor

Diabetic Neuropathy

Reflux Neuropathy

Incontinence

Calcium (sharp),magneisum, uric acid,
cystine
1-5mm can be passed
Usually unilateral and gives purely
Most common tumor in children,
kidney symptoms
defects in tumor-suppressor on
chromosome 11
Leading cause of chronic renal failure
1/3 ppl on dialysis have Type 1
diabetes, 2/3 have Type 2
Flow of urine from bladder to upper
tract
Can lead to end stage renal disease
1)Stress: most common Ex:sneeze
2)Urge: spasm
3)Overflow: can’t fully empty bladder
4)Functional: bladder normal,
something else keeps them from going
to bathroom Ex: spinal cord injury

Primary (congenital)
Secondary (obstruction)
Associated with hypertension
Associated w/ aging, most
common in women

Dialysis-provides filtration and reabsorption (hemodialysis=blood moves from shunt into machine, 3x per week for
4 hours)(Peritonal dialysis= peritoneal membrane serves as semipermiable membrane, usually done at home during
night)
Endocrine System Differential Diagnosis
Gigantism

​Acromagly- thicker skull and jaw (occurs after joint plates fuse)
Hyperthyroidism

​Common cause=Grave’s disease
​Common symptoms=exopthalmos, goiter, heat intolerance, and anxiety
Hypothyroidism

​Very familial, 4X more likely in women
​Common symptoms=weight gain, cold intolerance, fatigue
​Myxedema- lots of fluid (would not pit), can look like fibromyalgia bc of muscle aches and trigger point
​tenderness, sparse hair, brittle nails, may have buffalo hump
Thyroid storm-dumps T3 and T4 into system -> causes tachycardia, fever, and agitation
Thyroid cancer

​Very treatable, most are benign (only 5% malignant and they normally dont metastasize)
​Palpation will be painless, unilateral, and in one spot
Parathyroid glands

​Maintain calcium levels between bone and blood
​Parathyroid cancer=can’t easily be distinguished from thyroid cancer
Renal glands

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receptor not binding to insulin as well, pancreas intact), hyperglycemia
​develops slowly, may have genetic predisposition, 85-90% of all diabetes
​Risk factors: overweight, over 45 yrs old, inactive, women who had a baby over 9ilbs, low HDL
​Gestational=associated with type 2, glucose intolerance w/ pregnancy, increased risk of diabetes later on, if
​continues >6 weeks after pregnancy
...
if
​ 70 repeat, if >70 eat meal/snack (always assume they will drop 50 mg/dL while exercising) ​
<
Obesity **Nursing/Allied health professions have greater risk of injury due to rising obesity trends**

​Underweight = <18
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5-24
...
9 Obesity = BMI of 30 or greater
Subcutaneous vs
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Abdominal obesity=most important factor in determining pre-diabetic state (1 out of 5 US adults have
metabolic syndrome), want to avoid fat around organs (especially liver)
Hormone regulation

we

​Fat=largest/most active endocrine organ, releases 50 hormones, Adiponectin=hormone that signals brain
​are full (as fat cell gets bigger, releases less of this)
More macrophages recruited with obesity, causing chronic inflammation

Lifestyle=big factor (obesity trends with US Pima Indians vs Mexican Pima Indians)
Epigenetics= We can change which genes we turn on and off by our activitity

Pathophysiology Exam 5 Review

Acute Neurologic Disorders
Neurons and Conduction of Impulses
• Neurons: highly specialized, non-mitotic cells which conduct impulses through the CNS and PNS
• Myelin sheath: insulates, speeds up conduction, formed by Schwann cells, Nodes of Ranvier
• Glial cells: astroglia, oligodendroglia, microglia, ependymal cells
• Regeneration of Neurons: neuronal cell body damaged = death of neuron; CNS = neurons do NOT
regenerate; PNS = neurons may be able to
• Conduction of impulses: depolarization (sodium influx)
repolarization (outward movement of potassium)

à generation of action potential à

à sodium – potassium pump moves ions into

their normal position; myelinated fibers: salutatory conduction = rapid conduction
• Chemical neurotransmitters: stimulated

à released into synaptic cleft; inactivated by enzymes or

reuptake; postsynaptic neuron dendrites or cells body depolarizes depending on neurotransmitters
• Neurotransmitters:
o Acetylcholine: (excitatory and inhibitory) located: neuromuscular junction, autonomic
nervous system (SNS and PNS), peripheral nervous system, CNS
o Catecholamines: (excitatory) present in the brain, norepinephrine: neuromuscular junction
and SNS, epinephrine: SNS, dopamine
o Seratonin: (excitatory) located in the CNS (brain) and GI; regulates behavior, attention,
digestive processes; implicated in mood changes
o Glutamate: (excitatory)
o Y-Aminobutyric acid (GABA): (inhibitory) located in brain
• Autonomic Nervous System:
o Involuntary, motor and sensory innervation: cardiac muscle, smooth muscle, glands,
sympathetic/parasympathetic, neural pathway: preganglionic fibers (in brain or spinal
cord)

à postganglionic fibers (outside CNS)

• Sympathetic Nervous System:
o “Fight or flight”; stress response, increase general level of activity: cardio, respiratory,
neurologic, Neurotransmitters: preganglionic fibers release acetylcholine (cholinergic);
postganglionic fibers release norepinephrine (adrenergic)
• Parasympathetic Nervous System:

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Surgical repair, OT/PT
afterwards
Cerebral Palsy
Motor impairment due to brain Speech, PT/OT, assistive
damage: intellectual function, devices, monitor
behavior, communication /
hearing/vision, alternate modes
speech, seizures, visual or
of communication
hearing deficits
Causes: genetic mutations,
abnormal fetal formation, brain
damage, difficult delivery,
hypoxia (ischemia)
Spastic paralysis: hyperreflexia
Dyskinetic: loss of
coordination with fine
movement
Ataxic: loss of balance and
coordination
Multiple Sclerosis (MS)
Progressive demyelination of MRI for diagnosis and
neurons in brain, spinal cord, monitoring
and cranial nerves
Research treatments: interferon
Cause: unknown
beta – 1b, glucocorticoids
S&S: blurred vision, diplopia, PT/OT
scotoma, weakness in legs,
Muscle relaxants
progressive weakness and
paralysis, paresthesia,
dysarthria, loss of coordination,
bladder / bowel / sexual
dysfunction, chronic fatigue
Parkinson’s Disease
Progressive degeneration in
Removal of cause if known
basal nuclei; imbalance
Dopamine replacement therapy
between excitation and
Anticholinergic drugs
inhibition
Speech/language, PT/OT
Excess stimulation affects
Treatment of respiratory or
movement and posture
urinary tract infections
S&S: resting tremors (“pill
rolling”), muscular rigidity,
difficulty initiating movement,
postural instability, decreased
flexibility, fatigue, lack of
facial expressions, propulsive
gait, bradykinesia
Amyotrophic Lateral Sclerosis Muscle wasting, progressive
Stem cell therapy under
(ALS)
degenerative disease affecting investigation
motor neurons
Moderate exercise and rest
Cause: unknown
Electronic communication
Cognition, sensory neurons,
devices
neurons of eye are unaffected Team approach
Loss of upper motor neurons: No specific treatment to slow
spastic paralysis and
degeneration
hyperreflexia
Loss of lower motor neurons:
Flaccid paralysis, decreased
muscle tone and reflexes
Myasthenia Gravis (MG)
Autoimmune disorder: autoDiagnostic tests: EMG, serum
antibodies to acetylcholine
antibody test, acetylcholine
receptors at NMJ
esterase inhibitor
S&S: muscle weakness in
Treatment: antiacetylcholine

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• Pathogenesis: abnormal activity of the SNS, gate control theory, reflexive muscle spasm
• Stages of CRPS:
o Stage 1 (acute): right after injury, weeks to 3 mo
...
, persistent pain and stiffness, trophic skin changes,
muscle atrophy, flexion contractures, pain exacerbated by stimulus, limb: edematous,
cool, cyanotic, mottled, hair loss, cracked brittle nails, skin cool to touch
o Stage 3: atrophic stage, ~6 mo
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preoccupation with objects, inflexible adherence to routines and rituals
• Screening tests: Childhood Autism Rating Scale (CARS), Checklist for Autism in Toddlers
(CHAT), Autism screening questionnaire, screening test for autism in 2 year olds
• Treatment: intensive behavior therapy
Attention Deficit Hyperactivity Disorder (ADHD)
• Inability to focus on one thing in all aspects of life impairing function; diagnosis (must have all 3):
inattention, hyperactivity, and impulsivity
Tourettes Syndrome
• Characterized by tics; tics: involuntary, rapid, repetitive, and stereotyped movements of individual
muscle groups
• Transient tic disorder: do not persist for more than 1 year vs
...
chronic multiple tics: several chronic motor tics vs
...
, focus of worry will shift between things
Obsessive-Compulsive Disorder (OCD)
• Persistent, recurring thoughts and obsessions, obsessive behavior with repeated behavios
Panic Disorder
• 3 types of attacks: unexpected, situational, and situationally predisposed
Post Traumatic Stress Disorder
• Follows exposure to a traumatic event; 3 symptoms: relive the disaster, avoidance behavior,
emotional detachment from others

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