Clinic Entrance Exam: Western

Front 1

4 tissue types

Back 1

Epithelial
Muscle
Connective
Nervous

Front 2

Muscle tissue

Back 2

:contract for Movement & Support
- Skeletal muscle > voluntary (works when you want it to)
- Cardiac Muscle > only found in the heart, involuntary
- Smooth Muscle >  involuntary (works all the time)

Front 3

Epithelial tissue

Back 3

Lines our organs > ex. Stomach lining, skin

Front 4

Connective tissue

Back 4

:connects, supports, and protects other tissues
- ligaments, tendons, cartilage, bone, blood, fibers (organ walls)

Front 5

Nerve tissue

Back 5

- Gives signals to muscles, informs us of environmental conditions (hot, cold, *humid)
- ex. Brain, Spinal Cord, Nerves

Front 6

Nucleus

Back 6

The nucleus (most obvious organelle eukaryotic cell) -A membrane-bound organelle surrounded by a dble membrane. It communicates with surrounding cytosol via numerous nuclear pores. Inside: DNA responsible for providing cell with unique characteristics. The DNA is similar in every cell of the body, but depending on the specific cell type, some genes may be turned on or off - that's why a liver cell, muscle cell, + fat cell r different. When a cell is dividing, the DNA and surrounding protein condense into chromosomes that are visible by microscopy. The prominent structure in the nucleus is the nucleolus which produces ribosomes, which move out of the nucleus to positions on the rough ER where they are critical in protein synthesis

Front 7

Endoplasmic reticulum

Back 7

Throughout the eukaryotic cell, especially those responsible for the production of hormones and other secretory products, is a vast amount of membrane called the ER - a continuation of the outer nuclear membrane - some areas look "smooth" and some appear "rough." The rough ER = presence of ribosomes on the membrane surface. Smooth ER is important in the synthesis of lipids and membrane proteins. Rough ER is important in the synthesis of other proteins. Information coded in DNA sequences in the nucleus is transcribed as messenger RNA which exits the nucleus through small pores to enter the cytoplasm. At the ribosomes the messenger RNA is translated into proteins which are then transferred to the Golgi in "transport vesicles" where they are further processed and packaged into lysosomes, peroxisomes, or secretory vesicles

Front 8

Golgi apparatus

Back 8

: a membrane-bound structure with a single membrane - a stack of membrane-bound vesicles that are imp in packaging macromolecules for transport elsewhere in the cell. The stack of larger vesicles is surrounded by numerous smaller vesicles containing those packaged macromolecules. The enzymatic or hormonal contents of lysosomes, peroxisomes and secretory vesicles are packaged in membrane-bound vesicles at the periphery of the Golgi apparatus.

Front 9

Cytoskeleton

Back 9

helps to maintain cell shape, but the primary importance is cell motility. The int mvmnt of cell organelles, as well as cell locomotion and muscle fiber contraction could not take place without the cytoskeleton, an organized network of three primary protein filaments: microtubules, actin filaments, and intermediate fibers. (abundant F-actin stress fibers)

Front 10

Lysosomes

Back 10

contain hydrolytic enzymes necessary for intracellular digestion. In white blood cells that eat bacteria, lysosome contents are carefully released into the vacuole around the bacteria and serve to kill and digest those bacteria. Uncontrolled release of lysosome contents into the cytoplasm can also cause cell death (necrosis).

Front 11

Peroxisomes

Back 11

responsible for protecting the cell from its own production of toxic hydrogen peroxide. As an example, white blood cells produce hydrogen peroxide to kill bacteria. The oxidative enzymes in peroxisomes break down the hydrogen peroxide into water and oxygen.

Front 12

Mitochondria

Back 12

provide the energy a cell needs to move, divide, produce secretory products, contract - in short, they are the power centers of the cell. They are about the size of bacteria but may have different shapes depending on the cell type. Mitochondria are membrane-bound organelles, and like the nucleus have a double membrane. The outer membrane is fairly smooth. But the inner membrane is highly convoluted, forming folds called cristae. The cristae greatly increase the inner membrane's surface area. It is on these cristae that food (sugar) is combined with oxygen to produce ATP - the primary energy source for the cell.

Front 13

Ribosomes

Back 13

At the ribosomes the messenger RNA is translated into proteins which are then transferred to the Golgi in "transport vesicles" where they are further processed and packaged into lysosomes, peroxisomes, or secretory vesicles

Front 14

Pathology def

Back 14

Structural and Functional Abnormalities that get ​expressed as Diseases

Front 15

Cell injury occurs when...

Back 15

- the ability of the cell to ADAPT to change IS exceeded

Front 16

Common causes of cell injury

Back 16

1. O2 Deprivation = HYPOXIA
2. Chemical Agents
3. Infectious Agents (virus,bacteria)
4. Immunological rxns
5. Nutritional Imbalance
6. Aging
7. Physical Agents (trauma, burn)
8. Genetic defects (sickle cell)
HYPOXIA = O2 Deprivation
ISCHEMIA = dec. blood flow

Free Radical Injury  to cells by ROS = REACTIVE O2 SPECIES (as a form of cell injury)
 
ROS include (molecules with unpaired e-‘s) = O2 -, H2O2, OH.

Front 17

CELLULAR ADAPTION – Adaptive Responses (name + define 5)

Back 17

1. ATROPHY = decrease in size of cell (or organ)
2. HYPERTROPHY = increase in size of cell
3. HYPERPLASIA = increase in # of cells
4. METAPLASIA = replacement of one cell type with another
5. DYSPLASIA = cells of all diff. sizes and shapes – not uniform,disordered

Front 18

Necrosis

Back 18

IRREVERSIBLE  cell injury – cell injured beyond repair (involves enzymatic digestion of the cell

Front 19

Apoptosis

Back 19

Programmed Cell Death – suicide

Front 20

Inflammation

Back 20

Protective response to eliminate the cause of cell injury

Front 21

Cardinal fx of inflammation

Back 21

1. Rubor = Redness
2. Calor = Heat
3. Dolor = Pain
4. Tumor = Swelling
5. Functio laesa = Loss of Function

Front 22

Main components of acute inflammation (vascular + cellular changes)

Back 22

1. Vascular Changes  - vasodilation, increase in vascular permeability
2. Cellular Changes -  Immigration of WBC’s out into damaged tissue

Front 23

Process of leukocyte extravasation

Back 23

1. MARGINATION & ROLLING – WBC’s move to wall and stick
2. ADHESION & TRANSMIGRATION – WBC’s stick and crawl out gaps bet epith cells.
3. CHEMOTAXIS & ACTIVATION – WBC’s drawn to damaged area and release ​lysosomal enzymes
4. PHAGOCYTOSIS & DEGRANULATION – WBC’s gobble up bacteria & damaged cells ​and degrade them by enzymatic reaction

Front 24

Chemical mediators of inflammation

Back 24

1. Vasoactive amines – including Histamine, Serotonin
2. Neuropeptides (substance P)
3. Hageman Factor
4. Plasma Proteases –
a. Plasminogen activator
b. Kinin system – inc. bradykinin
c. Clotting system
d. Complement system
5. Arachidonic Acid Metabolites
a. Prostaglandins
b. Thromboxane A2
c. Leukotrienes
d. Lipoxins
6. Platelet Activating Factor
7. Cytokines… a bunch here, incl inflam. response TNF & IL-1
8. Nitric Oxide
9. ROS (reactive oxygen species)
10. Lysosoma constituents (proteases)

Front 25

Outcomes of acute inflammation

Back 25

RESOLUTION--- SCARRING OR FIBROSIS--- PROGRESSION TO CHRONIC INFLM.
(Characterized by more macrophages & lymphocytes - Acute more neutrophils)

(Tissue Repair: Regeneration of injured tissue OR replacement by fibrotic scar tissue)

Front 26

Purulent, sanguineous, catarrhal exudates

Back 26

*Purulent: contains PUS = neutrophils + necrotic cells + fluid,   (also dead bacteria)
*Sanguineous - bloody
*Catarrhal - Mucus (tends to nose + throat)

Front 27

Transudate

Back 27

transudate - a fluid substance that has passed through a membrane or has been extruded from a tissue; in contrast to an exudate, it is of high fluidity and has a low content of protein, cells, or solid materials derived from cells.

Front 28

Exudate

Back 28

exudate -a fluid with a high content of protein and cellular debris which has escaped from blood vessels and has been deposited in tissues or on tissue surfaces, usually as a result of inflammation.

Front 29

4 components of tissue repair

Back 29

1. Formation of New Blood Vessels
2. Proliferation of Fibroblasts
3. Depositition of ECM
4. Reorganization of Fibrous Tissue into a SCAR
*(FIBROSIS-repair by connective tissue)

Front 30

Causes of edema

Back 30

Edema: Increased Fluid in Interstitial Spaces
1. Increased Hydrostatic Pressure
2. Reduced Plasma Osmotic Pres. = HYPOPROTEINEMIA
3. Lymphatic Obstruction
4. Sodium Retention (in kd's)
5. Inflammation (increased permeability of vessel wall)

Front 31

Hemorrhage

Back 31

Extravasation of Blood due to a Ruptured Blood Vessel

Front 32

Know PROCESS OF HEMOSTASIS (blood clot formation

Back 32

1. Vasoconstriction
2. Platelet Aggregation
3. Formation of Fibrin
4. Cementing of Fibrin and platelets into a Clot

Front 33

Thrombosis Definiton + 3 main causes

Back 33

THROMBOSIS: Formation of Blood Clot in an Uninjured Vessel: interaction of vessel wall, platelets, and coagulation factors (grp of plasma proteins) in plasma (same interaction as hemostasis)
 
THE 3 MAIN CAUSES
1. Endothelial Injury
2. Alterations in Normal Blood Flow
3. Hyper coagulability

Front 34

Embolism (embolus) vs thrombus

Back 34

Embolism: Detached intravascular solid, liquid, or gaseous mass carried ​by the bloodstream to a distant site
Thrombus: The formation or presence of a blood clot in a blood vessel. (if breaks off: thromboembolism)

Front 35

Infarct

Back 35

Infarct- an area of Ischemic Necrosis caused  by Occlusion of Arterial Supply or Venous ​drainage

Front 36

Shock (process + 1st aid tx)

Back 36

SHOCK:  caused by Systemic HYPO perfusion du2 Decreased Cardiac Output or Decreased ​    Circulating Blood Volume
Types:
1. Cardiogenic
2. Hypovolemic
3. Septic
4. Neurogenic
5. Anaphylactic
*raise legs, keep warm, stop external cause (bleeding), Check pulse, be ready to resuscitate

Front 37

2 types of immunity (cellular + humoral)

Back 37

2 TYPES OF IMMUNITY:
1.) Humoral Immunity – B Lymphocytes make antibodies that bind to antigen, activates response
2.) Cellular Immunity – T-Lymphocytes (T-cells) recognize antigen and produce cytokines

Front 38

Types of immunity cells (focus on CD4, CD8)

Back 38

1. B-Lymphocytes – Bone marrow derived, produce antibodies (immunoglobulins) and form memory cells for future recognition of Acquired Immunity
2. T-Lymphocytes – Thymus derived, attach to antigen and present to B-cells
a. T-Helper cells = CD4 lymphocytes – express CD4, secrete cytokines to activate other cells, and present to B-cells
b. T-Supressor/cytotoxic cells (CD8 cells) – express CD8, bind & kill antigen​ directly
3. Phagocytes – neutrophils & monocytes, non-specific
a. Macrophages – help digest antigen for T-cells
4. Dendritic cells – in CNS lymphoid tissue, also help present antigen to CD4 cells
5. Natural Killer (NK) cells – innate (no need to recognize to react)

Front 39

Antibodies - source/types/main fx

Back 39

ANTIBODIES = Immunoglobulins produced by B-lymphocytes that bind to antigen (proteins, polysaccharides, nucleic acids)  
1. IgA – found in mucous secretions, early antiviral/antibacterial defense
 
2. IgE – allergic response (mostly respiratory and GI mucous secretions)
 
3. IgD – unclear what its for
 
4. IgM – 1st one formed after 1o exposure to new antigen (bacterial, viral, toxin), activates compliments
 
5. IgG – produced after 2 o exposure, most prevalent, protects from b,v, tox

Front 40

Human lymphocyte antigen

Back 40

HLA = human leukocyte antigen complex is a specific type of a Histocompatibility molecule, they cause problems with organ transplants cuz they are recognized by NK cells…. Autoimmune disease are linked to certain HLA types (ex Type I Diabetes)

Front 41

Cytokines effects

Back 41

CYTOKINES – 5 Categories, classes)
 
MEDIATE Innate Immunity – NK cells,IL-1, TNF
REGULATE lymphocyte growth, activation & differentiation (specific)
ACTIVATE inflammatory cells like TNF, -interferon
RECRUIT inflammatory cells
STIMULATE Hematopoiesis = blood cell production in marrow - wbc, lymphocytes, neutrophils, eosinophils

Front 42

Type 1 hypersensitivity reaction (pathologic immunologic response)

Back 42

1.  Type I Hypersensitivity – Immediate hypersensitivy
​- response of IgE antibody to presence of antigen
​- IgE binds with antigen on mast cells and causes release of histamine
 
ANAPHYLAXIS is a severe Type I Hypersensitivity response

Front 43

Type 2 hypersensitivity reaction (pathologic immunologic response)

Back 43

Type II – circulating IgM or IgG binds specifically to body antigen​ and causes death or damage of cells (mostly rbc’s))

Front 44

Type 3 hypersensitivity reaction (pathologic immunologic response)

Back 44

Type III – deposition of circulating A:A complexes that causes ​  ​   inflammatory response in vessel walls​(A:A = antibody:antigen)

Front 45

Type 4 hypersensitivity reaction (pathologic immunologic response)

Back 45

Type IV -  sensitized T-lymphocytes contacting an Antigen

Front 46

Neoplasia

Back 46

NEOPLASIA  - Permanent alteration in normal cellular growth patterns, neoplastic cells don’t respond normally to signals controlling growth and they proliferate excessively in a poorly regulated manner

Front 47

Types of neoplasias

Back 47

Benign - margins well defined, good differentiation (looks like cells of origin), slow growth (except uterine), very little mitosis (divisions), NU: cytoplasm ratio (normal to sl increase)

Malignant: poorly defined margins, poor differentiation, metastasis invades surrounding tissue, many rapidly dividing cells

Front 48

Mutation, teratogen + carcinoma in situ

Back 48

*Mutation: Permanent change in DNA
*Teratogen:  factors that induce abnormal embryo development
*Carcinoma in situ: a non-invasive malignancy

Front 49

Tumor grade vs scale

Back 49

*GRADING of a tumor is an estimate of aggressiveness or level of malignancy (Based on the microscopic appearance of cancer cells)
* SCALE - how much cancer has grown + spread

Front 50

Virus definition

Back 50

– obligate intracellular agents that need a host cell’s machinery for replication

Front 51

3 main shapes of bacteria

Back 51

Know the 3 main shapes of bacteria:
 
1. cocci – round
2. bacilli – rod
3. spirochete – spiral
*Some bacteria produce exotoxins and endotoxins that can damage human cells.

Front 52

Formation of an atheroma / plaque formation

Back 52

Atheroma:  a fibrofatty plaque  (also a plaque is a fibrofatty atheroma!)
*accumulations of WBC's esp macrophages that have taken up oxidized low-density lipoprotein (LDL). After they accumulate large amounts of cytoplasmic membranes (with associated high cholesterol content) they are called foam cells. When foam cells die, their contents are released, which attracts more macrophages and creates an extracellular lipid core near the center to inner surface of each atherosclerotic plaque. Conversely, the outer, older portions of the plaque become more calcific, less metabolically active and more physically stiff over time

Front 53

Atherosclerosis

Back 53

the formation of atheromas in the intima of large arteries

Front 54

Risk factors for atherosclerosis

Back 54

*Hyperlipidemia
*Hypertension (Hypertension:  bp > 140 systolic, 90 diastolic)
*Cigarette Smoking
*Diabetes
*Inflammation

Front 55

Significance of atherosclerosis

Back 55

- Occlusion of vessels resulting in ischemia
- Damage to the Media (smooth muscle cells & external elastic lamina) causing aneurysms
- Plaque disruption causing formation of thrombi (fixed) and emboli (floating)

Front 56

Main components of Plaques

Back 56

1. Cells
2. Extracellular Matrix (ECM)
3. Lipid

Front 57

Pathogenesis of plaque formation

Back 57

- Endothelial injury
- Accumulation of lipids
- Smooth muscle cell proliferation
- Oxidation of lipids

Front 58

Components of BP

Back 58

Components of (arterial) bp:  = Cardiac Output (CO) X Peripheral Resistance (PR)

NOTE: CO = the amount of blood pumped out of a ventricle per minute

Front 59

2 Factors that can cause increased Cardiac output

Back 59

2 Factors that can cause increased CO:
1.  Increased Heart Rate/force
2.  Increased Blood Volume

Front 60

Physiology of the Renin-Angiotensin System:

Back 60

Renin-Angiotensin System:
 
- Decreased Kidney blood flow causes secretion of Renin in the Kidney
- Renin converts Angiotensinogen into Angiotensin I
- Angiotensin I is converted to Angiotensin II by Angiotensin Converting Enzyme (ACE)
- Angiotensin II causes Vasoconstriction and promotes Na and Water retention

Front 61

Effects of Hypertension:

Back 61

-  Atherosclerosis – formation of atheromas in the intima of arteries occuring in arteriosclerosis
-  Cardiac Hypertrophy
-  Renal Failure
​-  Arteriolosclerosis – thickening hardening loss of elasticity of arteriole walls

Front 62

Vasculitis vs aneurysm vs varicosity

Back 62

*Vasculitis is an inflammatory dx of the blood vessels, & can be caused by immune mediated inflammation & direct infection of the blood vessels.
*aneurysm-an abnormal local dilation of a blood vessel
*Varicose Veins:  abnormally dilated, tortuous scarred veins from prolonged increased venous ​     pressure and loss of vein wall support

Front 63

Hypertension definition

Back 63

Hypertension:  bp > 140 systolic, 90 diastolic

Front 64

Congestive HT failure + compensatory mechanisms

Back 64

Heart Failure:
- Develops when the heart cannot maintain circulation due to extra work demand or a damaged heart muscle
Chronic Heart Failure = Congestive Heart Failure (CHF)
 
Compensatory mechanisms in heart failure:
 
1. Increased Heart Rate
2. Ventricular Hypertrophy
3. Dilation of the heart chambers
4. Activation of the Renin-Angiotensin cascade

Front 65

Left heart failure

Back 65

Left Heart Failure:  
• Results in:
o Pulmonary Hypertension
• Due to:
* blood backing up into the pulmonary circulation
* poor perfusion of tissues in the body due to inadequate CO

Front 66

Right heart failure

Back 66

Right Heart Failure:  
• Results in:
* Enlarged Liver (Hepatomegally)
* Peripheral Edema
* Jugular Vein Engorgement
Due to: Blood backing up into the Superior and Inferior Vena Cava

Front 67

Ishcemic heart diseasevs angina

Back 67

ISCHEMIC HEART DISEASE  ischemia is local & temp lack of blood supply to an area d/t obstruction of circulation
*Angina Pectoris:  Intermittent chest pain caused by intermittent myocardial ischemia, a relative xu of oxygen to

Front 68

Pathogenesis of Ischemic Heart Disease

Back 68

Pathogenesis of Ischemic Heart Disease:
– Atherosclerosis of the Coronary Arteries..
– Causes Thrombosis and Vasospasm resulting in..
– Occlusion of the Coronary Arteries
(complete occlusion results in Myocardial Infarction MI)

Front 69

Myocardial infarction

Back 69

Myocardial Infarction: an area of myocardial necrosis caused by local ischemia due to occlusion of ​    a coronary artery by a thrombus

Front 70

Anemia

Back 70

Anemia: reduction in the O2 carrying capacity of the blood usually due to decreased RBC’s, less than 6gm hemoglobin/100ml blood. Not a dx, but a symptom of vaious dx

Front 71

Mst common causes of anemia

Back 71

1. Blood loss  chronic blood loss anemia is d/t blood loss in the GI tract, urinary tract or uterus
2. Increased destruction of RBC’s  hemolytic anemia   can be caused by automimmune or mechanical damage of RBCs, RBC membrane alterations, defective hemoglobin synthesis
3. decreased production of RBC’s
can also be from iron xu  low iron intake, poor iron absorption, increased iron needs, chronic blood loss

Front 72

Thrombocytopenia

Back 72

Thrombocytopenia  decreased platelets (thrombocyte=blood platelet, penia = lack))  that leads to bleeding, common w/ bone marrow neoplasia, bone marrow supression or autoimmune destruction of platelets

Front 73

Dyspnea, hemoptysis, atelectasis definitions

Back 73

*Dyspnea  difficult breathing
​*Hemoptysis coughing up blood
​*Atelectasis absence of gas from all parts of the Lungs (ateles=imperfect, ektasis=expansion)
*plearisy: is inflammation of the pleura, symptom is stabbing chest pain with coughing or breathing
*asthma: • Bronchospasm • Airway inflammation IgE • Edema

Front 74

Splenomegaly + hepatomegaly

Back 74

*enlarged spleen; complication is spleen rupture
*enlarged liver

Front 75

Lymphocytosis

Back 75

Lymphocytosis:
• increased lymphocytes
• a response to viral infections

Front 76

Eosinophilia

Back 76

Eosinophilia:
• increased eosinophils,
• a response to hypersensitivity (allergy) and parasite infections

Front 77

Neutrophilic Leukocytosis

Back 77

Neutrophilic Leukocytosis:
• increased neutrophils
• a response to bacterial infection

Front 78

Neutropenia

Back 78

Neutropenia - decreased neutophils:
• predisposes to bacterial infections  
• when severe is known as agranulocytosis

Front 79

Leukopenia

Back 79

decreased WBCs  (in circulating count

Front 80

Leukocytosis

Back 80

increased WBCs  (in circulating count

Front 81

Obstructive lung disease is characterized by

Back 81

• decreased expiratory flow rate due to increased airway resistance (airway narrowing) and/or
• decreased outflow pressure due to loss of lung elastic recoil 

Front 82

COPD mixture of:

Back 82

• asthma,
• chronic bronchitis and
• emphysema

Front 83

Chronic bronchitis vs asthma

Back 83

*Bronchitis: • bronchial mucosal inflammation with mucous gland hyperplasia (abnormal increase in normal cells) & mucus hypersecretion;  
• daily productive cough for 3 months in two consecutive years;  
• common in cigarette smokers

*Asthma- Caused by:
• Bronchospasm
• Airway inflammation IgE
• Edema
Inflammation can be triggered by:
• Hypersensitivity response to antigen
• Inflammatory response to:
o irritants
o exertion
o cold air
o infections

Front 84

Pneumonia + consolidation

Back 84

Pneumonia - infective inflammation & consolidation of the lung
*consolidation = solidification into a firm, dense mass - in reference to a region of lung tissue that, normally compressible, has filled with liquid. Alveolar space containing liquid rather than gas - Fluid can be pulmonary edema, inflammatory exudate, pus, inhaled water, or blood (lobar pneumonia - referred to as consolidation)

Front 85

Acute pneumonia + cause

Back 85

Acute Pneumonia:
• caused by pyogenic bacteria; (pus producing)
• has four stages:
1. congestion,
2. red hepatization,
3. gray hepatization,
4. resolution

Front 86

Atypical pneumonia + cause

Back 86

Atypical Pneumonia: is infective inflammation & consolidation of the Lung & is caused by viruses, mycoplasma, chlamydia; AKA “walking pnemonia

Front 87

TB + cause

Back 87

TB is characterized by caseous granulomas formed by cell mediated hypersensitivity response to the mycobacterium tuberculosis bacteria

Front 88

Menieres disease

Back 88

Meniere’s Dx  severe vertigo, hearing loss, tinnitis, fullness/pressure

Front 89

Tinnitus, rhinisitis, sinusitis, epiglottitis, laryngitis

Back 89

Tinnitus  ringing
rhinisitis  nose
sinusitis sinus
pharyngitis  pharynx
epiglotitits  epliglotis
laryngitis larynx

Front 90

Acute vs serous otitis media

Back 90

56.​otitis externa  inflm of external ear canal
​*acute otitis media  inflm of middle ear
*serous otitis media  serous (fluid) going into middle ear

Front 91

Malignant lung neoplasia

Back 91

• most common cause of cancer death in both men & women in US;
• caused by carcinogens from cigarette smoke & industrial carcinogens;
• hemoptysis is characteristic symptom

Front 92

All the uria's...

Back 92

Polyuria – increased urination
Oliguria – decreased urination
Anuria – lack of urination
Nocturia – increased night urination
Dysuria – painful urination
Hematuria – blood in the urine
Proteinuria – protein in the urine
Azotemia – elevation of blood urea nitrogen (BUN) and creatinine due to decreased GFR.

Front 93

Chronic vs acute renal failure

Back 93

Renal Failure – when enough nephrons are non-functioning that blood filtration is not sufficient
​
​Acute –
• due to majority of nephrons suddenly not working,
• often happens with severe hypotension or hypovolemic shock
 
Chronic –
• due to progressive destruction of nephrons over a long time; occurs with:
o glomerular disease,
o tubulointerstitial disease &
o long standing hypertension

Front 94

Glomerular Disease

Back 94

caused by:
• injury from deposition of soluble circulating antigen-antibody complexes in the glomerulus or
• injury from antibodies reacting in situ (in position) within the glomerulus;  
results in:
• glomerular basement membrane (GBM) structural change;
leads to:
• abnormal protein loss and/or proliferation of endothelial or mesangial cells

Front 95

Acute pylelonephritis vs chronic glomeronephritis

Back 95

Acute pylelonephritis is a *bacterial infection of renal pelvis & kidney commonly caused by e.coli ascending infection of the lower urinary tract. Characterized by sudden onset of *fever, chills, flank pain, with pyuria (pus) and bacteriuria
Vs Glomerulonephritis is a type of kidney disease in which the part of your kidneys that helps filter waste and fluids from the blood
*Glomerulonephritis may be caused by problems with the body's immune system.
*Damage to the glomeruli causes blood and protein to be lost in the urine.

Front 96

Nephrotic vs nephritic syndrome

Back 96

Nephrotic Syndrome -  a clinical complex with:
• massive proteinuria,
• hypoalbuminemia,
• generalized edema,
• hyperplipidemia due to GBM damage and
• structural change that leads to leakage of protein

​Nephritic Syndrome - a  clinical complex with:
• hematuria,
• oliguria,
• azotemia,
• hypertension due to proliferation of glomerular cells with
• inflammatory reaction that damages capillary walls allowing leakage of  RBCs

Front 97

Diabetes mellitus causes renal injury - how?

Back 97

Diabetes mellitus results in Kidney disease from vascular disease
Causing:
• renal ischemia,
• glomerular damage, and
• increased susceptibility to UTI’s leading to pyelonephritis. Pyelo = renal pelvis

Front 98

Acute bacterial urethritis & cystitis cause by...

Back 98

Acute bacterial urethritis & cystitis (inlfm of UB) are most commonly caused by E. Coli; common in women, abn in men with normal urinary tracts and can lead to ascending infection

Front 99

Obstruction of urinary tract d/t, results in...

Back 99

Obstruction in the urinary tract is d/t stones, tumors, strictures, or compression & results in hydronephrosis ​(dilation of renal pelvis) with damage & atrophy

Front 100

GERD + esophageal cancer

Back 100

Gastroesophageal reflux disease
o occurs when the esophageal-gastric sphincter is incompetent leading to:
• reflux of gastric contents into the esophagus;
• can lead to Barrett Esophagus,
• the replacement of normal squamous mucosa with metaplastic columnar epithelium and
• esophageal adenocarcinoma

Front 101

Peptic ulcers cause...+ most commonly caused by...

Back 101

Chronic Gastritis and Peptic Ulcers are mostly caused by Helicobacter pylori infection that:
• induces an inflammatory & immune response,
• secretes enzymes (urease, proteases, lipases) &  toxins;
• enhances acid secretion;
• impairs bicarbonate;
• they are also caused by NSAIDs that inhibit prostaglandin secretion resulting in increased acid secretion & decreased bicarbonate and mucin production and inhibit healing

Front 102

5 Types of Diarrhea are:

Back 102

Diarrhea - an increase in stool mass, stool frequency or stool fluidity
5 Types of Diarrhea are:
Secretory – occurs when small & large intestines secrete more electrolytes and water than they absorb
Osmotic – unabsorbable, water-soluble solutes retain water in the intestinal lumen
Exudative – mucosal inflammation resulting in output of plasma, serum proteins, blood and mucus
Malabsorption – can be either secretory (bile acids, fatty acids) or osmotic (carbohydrates)
Deranged Motility – decreased intestinal retention time

Front 103

Hemorrhoids are...

Back 103

Hemorrhoids are varicosities of the anal & perianal submucosal venous plexuses

Front 104

Dysentery

Back 104

Dysentery -  low-volume, painful, bloody diarrhea.  
• Can easily result in dehydration & electrolyte imbalance.

Front 105

Intestinal Malabsorption Syndromes

Back 105

result in decreased absorption of fats, vitamins, proteins, ​ ​carbohydrates, electrolytes, minerals and water

Front 106

Crohns disease vs ulcerative colitis

Back 106

*Crohns is characterized by mucosal damage of the bowel, fissures of the bowel with formation of fistulae & abscesses d/t exaggerated & destructive mucosal damage (stricturing, penetrating (fistulae) + inflammatory) -
complications -bowel obstruction, perforation, hemorrhage (autoimmune- eye probs, intestinal stenosis, Can attack any part from mouth to anus)

Ulcerative colitis  continuous colon involvement starting in the rectum; edema & bleeding & ulceration of the colon mucosa; has increased risk of colorectal carcinoma (blood/pus, joint pain, N/V, skin lumps/lesions)

Front 107

IBSb / spastic colon

Back 107

IBSb  (spastic colon) occurs when the bowel muscle is hyperreactive or hyporeactive and presents with hypersensitivityto intraluminal distention of the bowel; can have diarrhea predominate or constipation or both mixed

Front 108

Chronic constipation

Back 108

Chronic constipation – hypothyroid, hypercalcemia, IBS, neurologic disorders, tumors, low fiber diet, lack of exercise, lack of fluids, laxative abuse

Front 109

Jaundice + icteric

Back 109

Jaundice: yellowing of skin, sclerae & other tissues caused by increased circulating bilirubin
Icteric: yellowish pigmentation caused by Jaundice=icterus

Front 110

Hepatic failure characterized by...

Back 110

Hepatic failure is characterized by jaundice, low albumin, high blood amonia & estrogen levels, bleeding d/t decreased production of clotting factors, encephalopathy

Front 111

Cirrhosis

Back 111

75. Cirrhosis: nodules of regenerated Liver cells with collagenous fibrosis preplacing normal Liver tissue

Front 112

Hep A, B, C

Back 112

77. Hep A  transmited fecal –oral rout, benign & self limited
Hep B  blood, sex, brith; acute or chronic, has carrier state, predisposes to Hepatocellular Carcinoma; dx w/antibody titers
Hep C  blood; hi rate of persistent chronic infection, carrier state;

Front 113

Cholelethiasis

Back 113

 gall stones; coomon in women, most common gall stone is cholesterol whcih occurs with cholesterol supersauturation of bile & bile statsis and can lead to gallbladder or bilary tree obstruction and cholecystitis

Front 114

Portal hypertension

Back 114

Portal hypertension  increased resistanc to portal blood flow with ascites hemmorrhoids, espohageal varices, & splenomegaly (sp is largest lymph vessel

Front 115

Hepatocellular carcinoma linked with -

Back 115

linked with Hep B, C, alcoholic Lr dx

Front 116

Most common referred pain in cholecystitis

Back 116

GB pain is in the RUQ, can raditate to right shoulder d/t diaphragmatic irritation

Front 117

Acute pancreatitis Causes

Back 117

acute pancreatitis  d/t pancreatic duct obstruction of direct injury to the pancreatic acinar cells; results in autodigestion of pancreatic cells

Front 118

Insulin actions

Back 118

*Insulin promotes glucose formation into glycogen & into fatty acids in Lr & inhibits Lr gluconeogenesis
 *Insulin promotes glucose upatke in the muscle cells
*Insulin promotes glucose transport in the fat cells and the formation fo triglycerides
* Insulin promotes uptake of amino acids into cells; formation of DNA RNA & transcripton of RNA to form proteins
* Insulin secretion  stimulated by increase in blood glucose levels, stops when blood glucose levels return to normal fasting levels = 80-90mg/dl. Nonfasting is 120-140mg/dl in 1st hour after eating

Front 119

Hyperthyroidism vs hypothyroidism

Back 119

Hyperthyroidism- excessive thyroid hormone secretion (elevated T3 and T4 levels)
• characterized by sweating, weight loss, tachycardia, palpitations, diarrhea, anxiety, tremor.
Hypothyroidism - underproduction of thyroid hormone
• characterized by fatigue, cold intolerance, hair loss, weight gain, depression, constipation

Front 120

Hashimoto thyroiditis

Back 120

Hashimoto Thyroiditis - an autoimmune inflammation and destruction of the thyroid gland
• presents with nontender firm goiter.  
• It is the most common cause of hypothyroidism in US.

Front 121

Addisons vs Cushing's

Back 121

Addisons: Deficiency of adrenocortical hormones (cortisol and aldosterone), is due to atrophy of the adrenal cortex, and is characterized by weakness, fatigue, increased skin pigmentation, diarrhea, cold intolerance, dizziness, weight loss, and hypoglycemia. Adrenal crisis is triggered by stress or trauma with adrenocortical hormone deficiency, and can lead to vascular collapse and death, and can be precipitated by abrupt withdrawal of corticosteroids.
*Cushing Syndrome: Excess cortisol, and is characterized by hypertension, truncal obesity, moon face, thin extremities, muscle wasting, thin skin, poor wound healing, easy bruising, stretch marks, hyperglycemia, decreased resistance to infection, mood swings, depression, psychosis. The most common cause is exogenous corticosteroid use.

Front 122

Goiter

Back 122

Abnormal enlargement in the thyroid gland

Front 123

Benign Prostatic Hyperplasia

Back 123

• Caused by dihydrotestosterone stimulating the growth of prostate cells, presents with:
o Difficulty in urinating
o urinary retention

Front 124

Cervical Intraepithelial Neoplasia (CIN)

Back 124

• a precancerous lesion of the cervix that is strongly associated with HPV infection;
• is the precurser to invasive cervical carcinoma;
• the screening test is the Pap smear

Front 125

Endometriosis

Back 125

• growth of endometrial tissue outside the uterine cavity;
• associated with pelvic pain and infertility

Front 126

Leiomyoma or Uterine Fibroid Tumors:

Back 126

• benign tumors of the myometrium that can cause (in perimenopausal women)
o dysmenorrhea,
o abnormal menstrual bleeding
*originate from smooth muscle tissue) that originates from the smooth muscle layer (myometrium) of the uterus

Front 127

Fibrocystic Breast Disease:

Back 127

• due to disturbances of estrogen/progesterone balance
• result in:
o hyperplasia of the lobules & ducts
o fibrous overgrowth of the breast stroma

Front 128

Ductal Carcinoma of the breast

Back 128

• is the most common type of breast cancer in US women.  
IDC invasive ductal carcinoma
*swelling of all or part of the breast
skin irritation or dimpling
breast pain
nipple pain or the nipple turning inward
redness, scaliness, or thickening of the nipple or breast skin
a nipple discharge other than breast milk
a lump in the underarm area
Risk factors: Increasing age, Personal history of benign breast disease, such as atypical hyperplasia, family history of breast cancer, First pregnancy after age 30, taking combination estrogen-progestin hormone replacement therapy after menopause
Genetic mutations that increase the risk of breast cancer, such as in the breast cancer genes BRCA1 and BRCA2

Front 129

Cerebral Infarction (Stroke)

Back 129

can be caused by ischemia or hemorrhage

Front 130

The most common malignant neoplasm of the CNS

Back 130

is a Metastatic Tumor.

Front 131

Dermatitis

Back 131

is inflammatory skin disease.

Front 132

Exposure to UV radiation predisposes to

Back 132

both Basal Cell Carcinoma & Squamous Cell Carcinoma of the Skin

Front 133

Malignant Melanoma

Back 133

presents as an irregular pigmented lesion of the skin

Front 134

Osteoporosis

Back 134

• characterized by generalized reduction in bone mass
• common in post-menopausal women and patients on prolonged corticosteroid therapy

Front 135

Osteoarthritis (OA) vs RA

Back 135

OA: Degeneration of articular cartilage with aging and wear & tear, inflammation is secondary to cartilage loss. It is characterized by joint stiffness and pain that is aggravated by use and may affect one or several joints, especially larger joints.
RA: An autoimmune inflammatory disease of the joints that destroys articular cartilage and bone. It is characterized by symmetric arthritis of small joints, and presents with fever, malaise and joint pain and stiffness. (morning stiff > 1 hr) - warm tender stiff
(RA: other sx: chest pain when taking breath (pleurisy), dry eyes + mouth (Sjogrens syndrome), eye burning, itching, discharge, nodules under the skin, numbness, tingling, burning hands/feet, sleep difficutlites

Front 136

Diabetes Mellitus definition

Back 136

DIABETES MELLITUS: syndrome of disordered metabolism and inappropriate hyperglycemia
• a chronic disease of carb, fat & protein metabolism
• resulting from inadequate action of the hormone Insulin
• characterized by high blood glucose

Front 137

Type 1 vs. Type 2 diabetes

Back 137

*Type 1 Diabetes Mellitus (Insulin Dependent): d/t immune destruction of pancreatic iselt beta cells resulting in xu of insulin secretion
• due to autoimmune damage to the insulin-secreting cells of the pancreas
 *Type 2 Diabetes Mellitus (adult onset): d/t peripheral tissue insulin resistence & deranged insulin secretion
• due to Resistance of cell membranes to the action of insulin
*peripheral tissue insulin resistance made worse by  hi levels of fatty acids, obesity, inacativity, sustained hyperglycemia & hyperinsulinemia.

Front 138

Complications of Diabetes Mellitus

Back 138

 glycosylation of proteins & collagen & by damage to cells by hyperglycemia with sorbitol accumualtion in the cell.  (Sorbitol damges schwann cells, which cover the nerve forming the mylin sheath)
• increased susceptibility to infection
• severe atherosclerosis with resulting tissue ischemia
• Kidney disease
• Peripheral neuropathy
• Cataract formation
• Retinal Damage

Front 139

Metabolic Syndrome + DM risk factors

Back 139

hyperglycemia, hyperinsulinemia, dilipidemia, hypertension & trunkal obesity

Front 140

Primary tissue at risk with DM, Complications

Back 140

*Macrovascular complications of DM include coronary artey dx, peripheral vascular dx & cerebrovascular dx (primary artherosclerosis)
 
*Microvascular complication of DM include damage to Ki, damage to retina & nerves causing retinopathy, neropathy, and peripheral neuropathy.
 
*Diabetics have decreased immune function & wound helaing
 
*Tight control of blood glucose levels in diabetics and delay and slow complications

Front 141

Hemoglobin A1c

Back 141

*common blood test used to diagnose type 1 and type 2 diabetes and then to gauge how well you're managing your diabetes

Front 142

Polycystic ovarian syndrome (POS)

Back 142

 insulin resistance & hyperinsulinemia causing increased production of testosterone and estrogen by the ovaries & results in anovulation, hirsutism, obesity

Front 143

Erectile dysfunction is most often d/t

Back 143

artherosclerosis of the artery of the penis

Front 144

Prostatits cause + sx

Back 144

-inflammation of prostate gland caused by infections of urethra & bladder
Sx: Pain or burning sensation when urinating (dysuria), Difficulty urinating, Frequent urination, particularly at night (nocturia), Urgent need to urinate, Pain in the abdomen, groin or lower back, Pain in the area between the scrotum and rectum (perineum), Pain or discomfort of the penis or testicles, Painful orgasms (ejaculations), Flu-like symptoms (with bacterial prostatitis)

Front 145

Benign prostatic hyperplasia definition (+ vs. Prostatic malignancy)

Back 145

*Benign prostatic hyperplasia is a proliferation oif the prostate cells d/t dihydrotestosterone & estrogen xs. Leads due dysuria, urinary hesitancy & urgency, incomplete emptying of BL, noctuira & urinary retention. FX 90% of men over 70. Most men have prostate CA when they die
*Carcinoma of prostate  most common malignancy in men.
Prostatic specific antigen test screening test for prostate CA

Front 146

Menopause, peri, post

Back 146

*Menopause 12 consecutive months w/o a period
 
*Perimenopause  late 30’s early 40’s, characterized by increasing estrogen & decreasing progesterone; rsults in hot flashes, night sweats, anxiety, mood swings, insomnia, menstrual changes, heart palpitations.
 
*Postmenopause  starts at menopause, can continue into old age, characterized by low estrogen, no progesterone.  Results in hot flashes, vaginal atrohy & bone loss.

Front 147

Cervical intraepithelial neoplasia

Back 147

Cervical intraepithelial neoplasia  CIN  precancerous legion of the cervix. Strong assoc w/ HPV infection, can progress to invasive cervial carcinoma. Screening test  PAP smear

Front 148

Menorrhagia + Metrorrhagia def

Back 148

*Menorrhagia  profuse & prolonged bleeding at the time of period
*Metrorrhagia  irregular bleeding in between peiods (metro=time)

Front 149

Dysfunctional uterine bleeding

Back 149

Dysfunctional uterine bleeding (DUB) often occurs d/t xs estrogen & inadequate progesterone stimulation of the endometrium. Common in puberty and perimenopause

Front 150

endometrial hyperplasia

Back 150

-endometrial hyperplasia occurs d/t xs estogen stimulation of endometrium & can lead to endometrial CA

Front 151

Factors involved in bone growth + maintenance

Back 151

Factors fx growth: calcium intake, reproductive hormone status, normal parathyroid gland function, and physical activity
*The same factors which encouraged bone formation in youth affect the maintenance of bone mass during the adult years

Front 152

Bone growth

Back 152

Longitudinal growth of a bone occurs at the epiphyses, or epiphyseal plates (end of long bone)
*The layer of periosteum builds concentric layers of new bone tissue on top of the existing ones. At the same time, the bone around the medullary cavity is resolved or eliminated so that the diameter can be enlarged continuously. Osteoblasts and osteoclasts are in charge of forming and resolving bone tissues, respectively
*osteoblasts, osteoclasts, osteocytes (buried/trapped in bones), and bone lining(retired osteoblasts) cells

Front 153

Skeletal muscle contraction - sliding filament mechanism

Back 153

mechanism used by muscles to contract.  The muscle shortens as a result of the sliding between two sets of filaments containing the proteins myosin and actin.
*contraction initiated by nerve impulse - carried along the axon of the motor n by the arrival of the n impulse and depolarization of the presynaptic membrane, causing fusion of the synaptic vesicles with the presynaptic membrane and exocitosis of acetylcholine into the synaptic cleft.

Front 154

Skeletal muscle contraction - Neuromuscular junction

Back 154

A signal to move a muscle travels from the CNS along a motor n in the form of a depolarization wave until it reaches a neuromuscular junction in the periphery. There, the motor n synapses with the targeted muscle cell, forming the neuromuscular jx, that is, a joining of a nervous cell and a muscle cell
*action potential, moving along the motor n carries depolarization wave to terminal buttons of the presynaptic neuron, which depolarize and release acetylcholine

Front 155

Skeletal muscle contraction - mineral + protein interactions

Back 155

mineral and protein interactions: action potential, potass, sodium flow

Front 156

Membrane depolarization + repolarization + action potential

Back 156

* cells are typically - charged, (stretched) (stretch receptors) - that open up pores so positively charged cells can enter. W/ enough pos charge, it changes electrical state and causes cell to fire “action potential” (sodium going in).   The ready state is polarized, action potential is “depolarization.” (sodium rushes in) - “repolarization” is the + charge cells (pumping sodium out) going out (3 K in for 2 Na out).  
*sodium potassium Pump involved in active transport - using ATP to move subst across membrane (against gradient)

Front 157

Autonomic nervous system:

Back 157

*manages unconcious behavior ie breathing, digestion, heart beat

Front 158

Sympathetic vs. Parasympathetic

Back 158

Sympathetic / fight + flight
• The heart rate increases
• Pyloerection (hair raises on end)
• Gut stops, possible defecation in your shorts
• Dialated eyes (take in more light, though focus suffers)
• Vasoconstricts in extremites > feed the brain
• Vasodialates in the core > feed the brain
• Increased respiration (breath shallow, fast, feel anxious)
*Parasympathetic / rest + digest

• heart rate decrease
• gut motility increases (boryborgymus), no poo in shorts.
• Pupils constrict
• Vasodialate in extrem
• Return to N respiration
***​     Para uses AcH, sympathetic uses norepinephrin (diff neurotransmitters)

Front 159

Neurotransmitter physiology

Back 159

*presynaptic (is firing) and *postsynaptic (whats being fired upon)

Front 160

Cranal nerves I-XII pneumonic for sensory/motor/mixed

Back 160

sensory/motor or both  > Some Say Mary Money, But My Brother Says Big Breast’s Matter More > sensory, sensory, motor, motor, both, motor, both, sensory, both, both, motor, motor

Front 161

Cranal nerves I-XII

Back 161

I: Olfactory/Smell
II: II Optic/Sight
III: Oculomotor/Moves eyes, up lid
IV: Trochlear/Moves the eyes
V: Trigeminal/Jaw, cheek, upper lip, lower lip
VI: Abducens /motor nerves supplying rectus on outer + lateral side of each eye- also called abducens
VII: Facial/facial expression
VIII: Auditory (aka acoustic, or vestibulo cochlear) Ear, hearing
IX: Glossopharengeal: mixed nerves + chiefly supply the pharynx, posterior tongue, and parotid gland--called also
X:Vagus/Digestion, poo, heart
XI: Accessory/SCM, traps
XII: hypoglossal/Below the tongue
Pneumonic: o o o to touch and feel a girls vagigi, oh heaven

Front 162

Thyroid hormones

Back 162

Thyroid h's manage metabolism -
makes T3 and T4
a) Thyroxine  T4 > prohormone and storage >  meaning it’s the precursor.  Need T4 to make T3.    requires days for maximum response.
b) Triodothyronine  T3 > influences growth, differentiation and metabolism.  2 to 4 X as potent as T4, acts quicker.  Considerd active hormone

Front 163

parathyroid hormone

Back 163

:  regulates the metabolism of calcium and phosphorus in the body > responsible for all muscle movement.

Front 164

Adrenal hormones/ + medullary hormones

Back 164

adrenal medullary glands secretes from inside: norepin + epineph, from surface (cortex) it secretes others (aldosterone, cortisol, anabolic hormones, sex hormones
*2 types of cortical steroids
a) Glucocorticoids > based on glucose > anabolic + sex hormones
b) mineralocorticoids > based on minerals like Ca2+, Phosphte, Na+, K+ > aldosterone, cortisol
• cortisol:  responsible for stress response > increases ration of norepineph and epineph (norepin respons for sympathetic nerv sys)
• aldosterone:  manages Urinary sodium output
• anabolic hormone:  build up muscle
• sex hormone:  test, estrog, progest ect…

Front 165

Pancreatic hormones

Back 165

sugar metabolism (pancreas has 2 spheres of action > endocrine/exo

> endocrine is ductless > deals with sugar metabolism
exocrine has ducts (dumping something out that doesn’t go into bld stream)
a) insulin > made by islet/beta cells:  causes glucose to be taken up from blood stream by cells.  (Used in mitochond/kreb cycle through arobic respiration to make ATP)
b) glucagon > made by alpha cells:  causes liver to dump out stored glucose called glycogen.

Front 166

ovarian hormones

Back 166

FSH > estrog > LH > progest > to ovulation
a) estrogen:  it’s peak - kicks off ovulation at the height of LH.   Estrogen causes LH to spike.  
b) Progesterone:  prepares and maintaines endometrium for implantation.   Promotes uterine musculature, vascular supply..    
*progesterone drops, allows for the sluphing.   Allows immuno suppression to allow invader to hook on (embryo cells)

Front 167

Testicular hormones

Back 167

produces 2ndary sex characteristics ie narrower hips, broader shoulders, facial hair ect..  Also resoponsible for formation of sperm and sexual drive.  7mg per day secretion from nuts, and .3g from ovaries.  Testosterone has anabolic (to build vs catabolism to destroy, together they are metabolism) effect in that it makes you bulk

Front 168

Melatonin

Back 168

a vertebrate hormone of the pineal gland that produces lightening of the skin by causing concentration of melanin in pigment-containingcells

Front 169

Hypothalamic and pituitary releasing factors

Back 169

• ​controls master gland (the pituitary which does thyroid stim hormone ect…) We have concious control of hypothalamus.
• ​Pituitary hormones:  ACTH, FSH, LH, MSH, GH (growth), TSH (thyr stim), PRL (prolactin), ADH > hypothal says “LH releasing factor” and pituitary releases LH
. Effects:  autocrine (affecting yourself), paracrine (you’re not affected by it but cells around you are).

Front 170

Formed elements of blood

Back 170

: (formed in red marrow from stem cells)
1. rbc > erythrocytes (transport oxygen and waste ie C02) > add and remove gases
2. wbc > leukocytes (defenders)
3. platelets > thrombocytes (clots)

Front 171

Fx of Formed elements of blood

Back 171

1. Input:  
a) brings immune system products (monocytes, lymphocytes, prostaglandins)
b) nutrients:  electrolytes, vitamins, minerals, glucose
c) oxygen
d) hormones/information substances
2. output:
a) metabolites (solid waste)
b) C02 (gaseous waste)
c) Heat (comes in and out)

Front 172

Cells of immunity

Back 172

- WBC’s > granulocytes:
- Neutrophils:  phagocytize bacteria
- Eosinophils: digest antigenic biproduct > strongly chemotaxic for digesting complex products of antigen/antibody reaction.
- Basophils:  release histamine which vasoD, heprin (anticoag) and seratonin and bradykinin (both vasoC)
- mast cells: similar to basophils, but found only in interstitial space in tissues.
- Agranulocytes:
- monocytes:  transform into tissue macrophages
- lymphocytes: T cells and B cells
- an antigen which is identified by a B cell which tags it for a macrophage to engulf it.

Front 173

Macrophages

Back 173

macrophages:  engulf and digest antigens

Front 174

B cells

Back 174

antigen specific immune cells with memory  > produce specific antibodies to an antigen (humoral immunity > liquid/phlegm/bile ie circulating) > they originate in Bone marrow (B) > don’t actually attack, just tag

Front 175

T cells

Back 175

3. T cells:  attack all foreign cells, originate in thymus (T) > cell mediated response

- T killer cells (cytotoxic), T helper cells (call B cells), T suppressor cells

Front 176

Antigens

Back 176

harmful substances foreign to the body

Front 177

Antibodies

Back 177

The body's reaction to antigens > the bodies tagging system for macrophages to eat

Front 178

External (pulmonary) respiration

Back 178

:  the gas exchange that happens in the lungs (RBC taking up 02, expiring C02) > exchange of air
1. movement of oxygen and carbon dioxide
2. alveolar-capillary membrane: more 02 in alveola, more C02 in capillaries
3. diffusion > using the concentration gradient, passive transport occurs.

Front 179

Internal (tissue) respiration

Back 179

:  cellular respiration (RBC’s releasing 02 for the tissue to use, and taking up C02 as waste) > exchange of gases
• movement of oxygen and carbon dioxide from tissue capillaries to tissue cells: higher concentration of C02 in cells, tends to diffuse out into the blood stream to an area of lower concentration (and a higher concentration of 02 in the blood stream)

Front 180

Cardiac circulation + cycle

Back 180

. Cardiac circulation (chambers and valves)
. Cardiac cycle:
-all venous return goes to vena cava > enters into right atrium >passes through tricuspid valve into right ventricle > out of pulmonary semilunar valve into pulmonary artery > into lungs > returns to heart through pulmonary veins > lft atrium > through bicuspid or mitral valve and empties into left ventricle > through aortic semilunar valve into systemic circulation.

Front 181

right sided heart failure

Back 181

:  backs up the venous return > causes edema of lower limbs, or pulmonary edema. (if right heart is not pushing blood into lungs, its not being pushed out of lungs, plasma will tend to diffuse out of capillaries into lungs, and alveolar space.)

Front 182

left sided heart failure

Back 182

will not get 02 to the tissues > causes fatigue, will turn blue

Front 183

Digestion + absorption: mouth

Back 183

mouth:  
- salivary amylase:  breaks CHO down in the mouth
- lingual lipase:  enzyme in from under T that breaks fat down

Front 184

Digestion + absorption: ST cells involved

Back 184

cells
- chief cells:   secrete pepsinogen, that on contact with the acid of the gastric juice, convert to the proteolytic enzyme pepsin
- parietal cells:  secrete HCl (hydrochloric acid)
- mucous cells:  secrete mucous which protects stomach lining from HCl

Front 185

Digestion + absorption: ST pepsin and intrinsic factor

Back 185

:  pepsin is an enzyme (in st) that breaks peptide bonds (proteins).  Intrinsic factor is a glycoprotein secreted by parietal cells of the gastric mucosa.  Has an important role in the absorption of vitamin B12 (cobalamin) in the intestine, and failure to produce or utilize intrinsic factor results in pernicious anemia.

Front 186

Digestion + absorption: ST regulation of secretion (information molecules)

Back 186

- gastrin:  major physiological regulator of gastric acid secretion. It also has an important trophic or growth-promoting influence on the gastric mucosa.  
- Secretin:  stimulates the pancreas to emit digestive fluids that are rich in bicarbonate which neutralizes the acidity of the intestines, the stomach to produce pepsin (an enzyme that aids digestion of protein), and the liver to produce bile.  
- GIP:  gastric inhibitory polypeptide > tells the pancreatic Beta cells to be ready for sugar “ turns on the receptor for the insulin production facilities. (then will make insulin)
- CCK:  cholecystikinin > tells GB to secrete bile
- Secretin turns on exocrine fx of panc, and GIP the endocrine fx of

Front 187

Digestion + absorption: Pancreas enzymes

Back 187

a) enzymes:
- pancreatic amylase and lipase:   breaks down CHO, lipase fats
- protease:  pepsin is a protease > enzyme that breaks down

Front 188

Digestion + absorption: liver fx + role of bile

Back 188

a) fxs:  detox, storage/production of glycogen, production of bile, chemical filtration of blood (kid is physical filtration)
b) bile:  both fat emulsifier, and metabolic end product (waste)
- function in the absorption of lipids:  bile makes fats water soluable > makes lipids transportable

Front 189

Gallbladder fx

Back 189

holds and excretes bile

Front 190

SI segments + mechanical/chemical fx

Back 190

- segments:  duodenum, jejunum, ileum
- function:  mechanical, chemical > soup of amino acid (break down product of protein), glucose (breakdown product of CHO), emulcified fats (breakdown product of lipids) end up in SI.  The chemical function of the SI is to transport the above from the lumen into either the bloodstream or the lymph (pulling stuff out that’s pure, leaving the stuff that’s impure).  Chemical fx:  chyme enters duod, and being blasted by pancreatic enzymes (lipase, protease, amylase), also:  diffusion X membrane into microvillai.

Front 191

LI segments + mechanical/chemical fx

Back 191

a) segments:  ileocecal valve, ascending colon, hepatic flecture, transverse colon, splenic flecture, descending colon, sigmoid colon, rectum, anus.
b) Function:  physically moving along bulk waste AND resorbing water.  Chemical absorption of trace minerals.

Front 192

Urinary arterioles (afferent vs efferent)

Back 192

A.  arterioles:  tiny arteries
1. afferent vs efferent:  afferent (towards the center), efferent (away from the center)

Front 193

Urinary nephrons structure

Back 193

Nephron:  a unit of fx in the kidneys which produce urine from a filtrate of blood.   job: to control concentration of urine.
1. structure:
- glomerulus:  the blood vessel that comes into the nephron
- bowmans capsule:  surrounds glomerulus and collects fluids
- proximal convoluted tubule:  reabsorbs 2/3 of the water and almost all nutrients from the filtrate.  Also secretes organic acids/bases.
- loop of henle:  water is sent back into lumen leaving highly concentrated urine
- distal convoluted tubule:  Sodium absorption by the distal tubule mediated aldosterone- which incr sodium reabsorption (so pulls water in too)
- collecting tubule:  catches all of the filtrate, enters renal pelvis, goes through ureter to the bladder.

Front 194

Urinary nephrons: glomerular filtration, tubular resorption + secretion

Back 194

*HBP in glomerulus forces small molecules from blood into bow mans capsule
*prox convoluted tubule- glucose, amino acids, ions, other useful subs. r actively transp from tubule into blood (water follows passively by osmosis)
*descending loop of henle- water diffuses out of tubule by osmosis
*ascending loop of henle- salts actively transp out of tubule, Walter can't follow becuz tubule walls impermeable
*distal convoluted tubule- K+ and H+ and other ions + certain lrg molecules r actively transp from blood into tubule, regulating pH + ionic concentration of blood
*collecting duct- as urine passes down duct, water moves by osmosis from duct into blood
*to renal pelvis + ureter

Front 195

More on Urinary nephrons: glomerular filtration, tubular resorption + secretion

Back 195

glomerular filtration is nonselective, tubular reabsorption is extremely selective. strategy is to push everything into the nephron and then selectively reabsorb salts, sugar and water that the body cannot afford to lose.This reabsorption is accomp bytransport systems embedded in the cell membranes of the epithelial cells + transport glucose, salts + other valuable nutrients back into the blood stream. In the distal convoluted tubule, the comp of urine is modified by tubular secretion-- various substances are secreted back into the nephron. These include urea and urobilin

Front 196

aldosterone and antidiuretic hormone

Back 196

*act on the distal parts of the nephron (distal convol tubule)
* if you were to eat salty food, the increased level of sodium in your blood str would trigger a dec in the amt of aldosterone by your adrenal cortex - causing dec reabsorption of sodium by the cells of the tubule and inc concentr of salt in the urine. Viceversa: a drop in blood sodium stim an incr in aldosterone prod which incr the reabsorption of sodium from the tubule.
*volume of blood is deter by its water content. Blood vol decr when too little water is reabsorbed from the nephrons back into the blood stream- which causes the blood to become too concentrated.  Receptors in the hypothalamus detect the incr in the blood's osmotic strength and direct the posterior pituitary to release antidiuretic h.
*Antidiuretic hormone increases the permeability of the distal portion of the nephron allowing more water to be reabsorbed from nephron back into blood stream which dilutes the blood and concentrates the urine.

Front 197

Juxtaglomerular apparatus

Back 197

The juxtaglomerular apparatus cells: cells near the glomerulus in the kidney. These cells are specialized cells that stim the secretion of the adrenal h, aldosterone, + play a major role in renal autoregulation
*regulates fx of each nephron, regulating renal blood flow and glomerular filtration rate.

Front 198

Renin-angiotensin

Back 198

BP regulation :  when kidney finds the BP is low, it releases renin > breaks angiotensinogen into angiotensin ​1.  ACE (angiotensin converting enzyme) converts angiotensin 1 to angiotensin 2, which causes more water to be pulled back in from the collecting ducts to the blood (elevating the BP)

Front 199

Ureters, UB, urethra def

Back 199

Ureters: connect the kidney to the bladder
Urinary bladder: holds urine
Urethra:  connects the urinary bladder to outside

Front 200

Male accessory sex glands

Back 200

a) seminal vesicles:  produce semen to protect sperm once it leaves penis = 2 membranous pouches (post to BL btwn this organ + rectum) Seminal vesicles prod secretions containin fructose, amino acids, mucus, + sml amts of sum vit. During ejaculation, these subst r added to the semen at the time spermatozoa are transp to ejaculatory ducts frm vas deferens. The fructose and other subst contained in seminal fluid provide nutri and protection 4 spermatozoa. All secretions added to the semen increase its bulk.
b) prostate:  closes urethra to keep pH in the urethra sperm friendly and produces prostatic fluid. (inf to the UB + int urethral orifice) It surrounds 1st portion of urethra = prostatic urethra, (+ is like a chestnut). prostate is covered by a dense fibrous capsule and consists of glandular units surround by fibromuscular tissue that contracts only during ejaculation. The glandular tissue consists of tubules which communicate with the urethra by minute orifices, The fx of the prostate gland is to secrete a thin, milky alkaline fluid that enhance spermatic motility
c) cowpers gland:  produces precum to neutralize the pH in urethra.

Front 201

Ovarian cycle (follicular phase 1st)

Back 201

a) follicular phase - preovulatory - about 12 days
i. 1st day of bleeding to day before preovulatory LH surge
ii. inc FSH in 1st half
1. initiates follicular development
iii. LH slowly rises 1-2 days after FSH rise
iv. E & P low
v. E rises 7 days before preovulatory LH surge
1. endometrial proliferation
vi. at this time, slow inc in LH and dec in FSH

Front 202

Ovarian cycle (ovulatory phase, 2nd)

Back 202

b) ovulatory phase - about 2 days
i. massive release of LH
ii. simultaneous great inc E
1. release of follicle 16-32 hours after initial surge - surge lasts 36-48 hours
iii. small inc FSH
iv. as LH rises, E falls
v. P continues to rise

Front 203

Ovarian cycle (luteal phase 3rd)

Back 203

c) luteal phase - postovulatory - 14 days
i. from lifespan of corpus luteum in ovary
1. supports ovary by secreting P
2. P causes coiling of endometrial glands and inc vascularity
ii. LH and FSH low - inc again with menstruation
iii. E lowers from pre and ovulatory highs
iv. both E & P dec in late luteal phase
1. endometrium becomes more edematous & necrotic, and bleeding occurs
2. PG may play role
a. vasoconstriction, necrosis
b. uterine contractions

Front 204

Ovaries structure

Back 204

ovaries structure: The ovaries are situated on the side of the uterus just below the finger like projections of the fallopian tubes The ovaries perform two main functions: production of female sex hormones -estrogen and progesterone, and the production of mature ova
estrogen is responsible for development and maintenance of all secondary sex characters such as breast, shape of the body, and maturity of the reproductive organs such as vagina, uterus, fallopian tubes, etc.

Front 205

CVA vs. TIA

Back 205

*Cerebral vascular accident, aka strokes, are disorders involving “sudden, focal interruption of cerebral blood flow, causing neurologic deficit.” They can be ischemic (80%), resulting from thrombosis or embolism, or hemorrhagic (20%), resulting from vascular rupture.

*A transient ischemic attack is an episode of non-traumatic focal loss of cerebra or visual function for <24 hours; TIAs are considered a precursor to stroke.

Front 206

Acute Eczematous Dermatitis (Eczema)

Back 206

Produces a red, papulovesicular, oozing, crusted lesion. Can be due to a Type IV hypersensitivity response to contact with antigen (Allergic Contact Dermatitis) or genetic susceptibility to environmental triggers (Atopic Dermatitis).

Front 207

Pustule, vesicle, macule, papule

Back 207

*Pustule: Superficial elevated lesion containing pus
*Papule: Solid elevated lesion less than 10mm
*vesicle: Circumscribed elevated lesion less than 5mm containing serous fluid
Macule: Flat discolored spot less than 10mm

Front 208

Alzheimer’s Disease

Back 208

Characterized by dementia (progressive memory impairment and cognitive deficits) and brain findings include neurofibrillary tangles, senile plaques, amyloid deposits.

Front 209

Parkinsons

Back 209

Progressive degeneration of the pigmented neurons of the substantia nigra that produce dopamine causing dysruption , of the dopaminergic pathways from the substantia nigra to the basal ganglia.

Front 210

Peripheral neuropathies

Back 210

A syndrome of sensory loss, muscle weakness & atrophy, decreased deep tendon reflexes, autonomic changes that can be caused by diabetes, nutritional deficiencies, toxic exposures or inflammatory conditions.

Front 211

MS

Back 211

Immune mediated demyelination in the CNS leading to failure of axonal function & neurological dysfunction.
>woman (20-40 yrs usu)
*MS is caused by damage to the myelin sheath, the protective covering that surrounds nerve cells. When this nerve covering is damaged, nerve signals slow down or stop.

The nerve damage is caused by inflammation -body's own immune cells attack the nervous system. This can occur along any area of the brain, optic nerve, and spinal cord.

Front 212

Myofascial Syndrome

Back 212

Characterized by distinct trigger point areas that become abnormally active and produce local and referred pain. It is initiated by acute strain cause by sudden overload or overstretching of muscle producing hyperexcitable foci in the skeletal muscles or fascia.

Front 213

Epilepsy / seizure

Back 213

Epilepsy is a medical condition that produces seizures that affect a variety of mental and physical functions.
*Myoclonic seizures: Are rapid, brief contractions of bodily muscles, which usually occur at the same time on both sides of the body. Occasionally, one arm or a foot.
*Tonic clonic: losing consciousness and falling down.
Stiffening of the limbs (the tonic phase) is followed by jerking of the limbs and face (the clonic phase).
*Atonic: Produce an abrupt loss of muscle tone. Other names for this type of seizure include drop attacks, astatic or akinetic seizures. head drops, loss of posture, or sudden collapse.
*absence: petit mal: Lapses of awareness, sometimes with staring, that begin and end abruptly, lasting only a few seconds. no warning and no after-effect.

Front 214

Tension, migraine, cluster H.A

Back 214

*Tension headaches
*Migraine headache
Classic migraine: 20%, aura
Common migraine
*Cluster headaches: The pain is excruciating and located around or behind one eye -like a hot poker in the eye - red, inflamed, and watery. The nose on the affected side congested and runny.

Migraine: Described as an intense, throbbing or pounding pain that involves one temple. (smtime located on forehead, around the eye, or at the back of the head). Usually unilateral

Front 215

Migraine triggers

Back 215

sx: N,V, aura, photophobia
triggers:
foods: Common offenders include alcohol, especially beer and red wine; aged cheeses; chocolate; aspartame; overuse of caffeine; monosodium glutamate
*hormonal changes
*stress, sensory stimuli,
Prodrome:
Constipation, Depression, Diarrhea, Food cravings, Hyperactivity, Irritability
Neck stiffness

Front 216

Sleep apnea

Back 216

When breathing stops during sleep for > 10 seconds, occurs > 20 times per hour causing hypoxia. Usually caused by upper airway obstruction

Front 217

h.a. red flag

Back 217

New headaches or changes in chronic headaches need investigation.

Front 218

Psoriasis

Back 218

Characterized by pink to salmon-colored plaques covered with silver-white loosely adherent scales. Sensitized T cells secrete cytokines and growth factors that cause inflammation and proliferation of keratinocytes.

Front 219

urticaria

Back 219

A Type I hypersensitivity response to antigens resulting in localized mast cell degranulation with release of histamine causing pruritic papules.

Front 220

bacterial vaginosis

Back 220

disruption of normal vaginal flora
-results in anaerobic bacterial overgrowth
-fishy smelling discharge

Front 221

Leukoplakia

Back 221

Leukoplakia are patches on the tongue, in the mouth, or on the inside of the cheek that occur in response to long-term irritation. Leukoplakia patches may also develop on the outer female genitals.
*smoking, etc

Front 222

Epiglottitis

Back 222

*dont use tongue compressor
Swelling of the epiglottis is usually caused by the bacteria Haemophilus influenzae (H. influenzae). It may also be caused by other bacteria or viruses related to upper respiratory infections.
*serious medical emergency: spasm may cause airway to close unexpectedly
***Epiglottitis begins with a high fever and sore throat. Other symptoms may include:
Abnormal breathing sounds (stridor)
Chills, shaking
Cyanosis (blue skin coloring
Drooling
Difficulty breathing (patient may need to sit upright and lean slightly forward to breathe)
Difficulty swallowing
Voice changes (hoarseness)

Front 223

aphthous ulcer vs herpetic lesion

Back 223

aphthous ulcer: affect the unattached mucosa, white or yellow and surrounded by a bright red area
herpetic lesion: It causes small, painful blisters commonly called cold sores or fever blisters.
*Red blisters that break open and leak, Small blisters filled with clear yellowish fluid, Several smaller blisters may grow together into a large blister, As the blister heals, it gets yellow and crusty, eventually turning into pink skin (sore throat, Fever, swollen glands)

Front 224

Hiatal hernia

Back 224

Hiatal hernia is a condition in which part of the stomach sticks upward into the chest, through an opening in the diaphragm.
*chest pain, heart burn, diff swallowing (infants w/ gastroesoph relux, px over 50)