Final Exam Patho Flashcards
what are the types of cell adaptation and give examples
- Atrophy- declining, cells revert to smaller size (ex: muscle atrophy/paralysis (low nerve simulation)/low nutrition/ischemia/ aging
- Hypertrophy- increasing in size (ex: hypertension= overused big heart/ weightlifting/ fever)
- dysplasia- disordered cell, deranged cell growth, functions differently, not the true adaptation of cell, abnormal change (ex: cervical cancer- change of cells in cervix)
- hyperplasia- increase in number of cells (breast tissue w/ pregnancy, keloid scar, BPH aka benign prosthetic hyperplasia)
- metaplasia - cells look different, one cell changes to another (Ex: Barrett’s esophagus/ GERD)
- neoplasia- new growth, lack adhesion to other cells, lack normal function (Ex: cancer - any time cells undergo mitosis = risk for cancer)
type of cell adaptation that is declining, cells revert to smaller size (ex: muscle atrophy/paralysis (low nerve simulation)/low nutrition/ischemia/ aging
atrophy
type of cell adaptation that is increasing in size (ex: hypertension= overused big heart/ weightlifting/ fever)
hypertrophy
type of cell adaptation that is disordered cell, deranged cell growth, functions differently, not the true adaptation of cell, abnormal change (ex: cervical cancer- change of cells in cervix)
dysplasia
type of cell adaptation that is the increase in number of cells (breast tissue w/ pregnancy, keloid scar, BPH aka benign prosthetic hyperplasia)
hyperplasia
type of cell adaptation where cells look different, one cell changes to another / replaced by another (Ex: Barrett’s esophagus/ GERD)
metaplasia
type of cell adaptation that is new growth (tumor), lack adhesion to other cells, lack normal function (Ex: cancer - any time cells undergo mitosis = risk for cancer)
neoplasia
type of cell injury that is reactive oxidative stress, antioxidants fight them off
(ex: uncontrolled diabetes- high glucose conc. , uncontrolled hypertension- high bp)
**all cause high O2 consumption
fever, cancer, radiation also can cause these!
examples of disorders that are associated with this type of cell injury included Alzheimers, atherosclerotic heart disease, cataracts, cancer, emphysema, aging
free radical
what is a free radical & what can protect against them?
it is a harmful agent.
antioxidants (vitamins such as A, E, C and minerals such as copper, zinc, selenium) protect against them!
antioxidants neutralize free radicals aka a harmful agent
type of cell death that is genetically programmed cell death, eliminates unwanted cells….. cells that resist this can give rise to cancer (ex: hashimoto’s causes gradual failure of thyroid gland bc of increased apoptotic cell death)
apoptosis
type of cell death that is caused by injury, it is a “messy” process of cell death, due to stressors or insults that overwhelm their ability to survive, irreversible, due to lack of oxygen. Brain liquifies (bacterial meningitis cross through blood brain barrier), lung tissue destroyed by TB becomes dense & cheese like, gangrene (fatal unless surgical debridement, amputation, antibiotics…EX of gangrene= clostridium perfringens which emits gas odor, anaerobic bacteria)
necrosis
trait expressed only when inheriting defective gene from BOTH parents, individual is homozygous for the abnormal gene, 25% chance that the offspring will be affected by the disease, 50% they will be a carrier… both parents have to be carriers (Ex: cystic fibrosis, sickle cell)
autosomal recessive
trait expressed whenever the gene is present from EITHER parent, any child who inherits the trait will develop this disease, 50% chance offspring will be affected (Huntington Disease or Marfan Syndrome aka tall or NF or Familial hypercholesterolemia)
autosomal dominant
trait that is expressed in any male that carries the affected gene. males are affects, females are carries! (Ex: klinefelters aka men have extra X, turner’s syndrome aka women missing an X)
X (sex) linked
type of cell injury that includes down syndrome, turner’s disease
genetic defects
monosomy of the sex chromosome, girl who has only 1 X chromosome, webbed beck, shield like chest with underdeveloped breasts, widely spaced nipples, imperfectly developed ovaries, hypothyroidism, short stature, female genitalia
Turner’s Syndrome
most common chromosomal disorder, intellectual disability, caused by trisomy 21
S&S: cognitive impairment, dysmorphic facial features, heart defects
Down syndrome
aka Martin Bell syndrome, most common cause of inherited cognitive impairment and second most common cause of genetically associated mental disabilities after trisomy 21.
S&S: autistic like behavior- flapping hands no eye contact, shyness, sensory integration difficulties, attention deficit, depressed affect, anxiety, learning disabilities, aggressive tendencies, mental delays, decreasing IQ with age
fragile X syndrome
one of most common male chromosomal genetic disorders, an extra X
S&S: physical & cognitive abnormalities. Lack of development of tests, gynecomastia (breast development), skeletal and cardiovascular abnormalities, lack of hair, decreased muscle mass, emotional issues/lack of learning disabilities that resembles autism, low bone density, difficult fertility/ED issues
Klinefelter syndrome
symptoms of systemic infection aka in the bloodstream
stage 3 (last) of acute inflammation that has symptoms including fever, pain, general malaise, lymphadenopathy, anorexia, sleepiness, lethargy, anemia, weight loss
symptoms of localized infection aka only one body part or organ is affected
Acute localized inflammation = pain, heat, redness, swelling, and loss of function
shift to the left WBC
bacterial, acute inflammatory process is occurring. Neutrophils & bands will be above normal range
shift to the right WBC
viral
what are the 5 cardinal signs of inflammation
- Rubor (Red)
- Dolor (pain)
- Calor (heat)
- Tumor (swelling)
- Loss of function
what stimulates a fever?
When bacteria or viruses invade the body and cause tissue injury, one of the immune system’s responses is to produce PYROGENS (substance that causes fever).
Pyrogens activate/release PROSTAGLANDINS to reset the hypothalamic temperature regulating center in the brain to a higher level.
what is a pyrogen & what chemical mediator is released to cause fever?
pyrogen- substances that cause fever
chemical mediator- cells (cytokines) or the bacteria (prostaglandins)
**pyrogens activate prostaglandins to reset the hypothalamic temperature regulating center in the brain to a higher level.
**An antipyretic agent = drug that brings down fever
meds that are antipyretic
Tylenol, ibuprofen, acetaminophen, aspirin
**NEVER give kids aspirin or any salicylate-containing products for fever
3 phases of wound healing process
primary intention: aka primary union, lease complicated type, simple rapid healing (ex: surgical wound), no missing tissue
secondary intention: when there is extensive loss of tissue within wound, repair is more complex. regeneration isn’t possible. substantial scar formation and thinning of epidermis occurs. wounds are highly susceptible to infection, complications, deformity (ex: decubitus ulcer)
tertiary: aka tertiary union, would is missing large amount of deep tissues and is contaminated. it’s cleaned & left open x4-5days before closure. may require packing of sterile gauze, drainage tube, commonly requires skin graft
type of wound healing that is the least complicated type, simple rapid healing (ex: surgical wound), no missing tissue
primary intention
type of wound healing when there is extensive loss of tissue within wound, repair is more complex. regeneration isn’t possible. substantial scar formation and thinning of epidermis occurs. wounds are highly susceptible to infection, complications, deformity (ex: decubitus ulcer)
secondary intention
type of wound healing where it’s missing large amount of deep tissues and is contaminated. it’s cleaned & left open x4-5days before closure. may require packing of sterile gauze, drainage tube, commonly requires skin graft
tertiary intention
what are the 4 types of immunity
- Innate immune response: immune responses that is our skin, mucus membranes, enzymes
- Adaptive immune response: immune response that once it has seen an antigen, it recognizes it & adapts to it to know how to deal with it next time. Ex: immunizations
a. humoral immunity (type of adaptive): B lymphocyte immunity
b. cell-mediated immunity (type of adaptive): T lymphocyte immunity - Active acquired immunity: type of immunity that is obtained through exposure to an antigen or through a vaccination that provides immunization. LONGER LASTING.
a. Ex: child develops this immunity after a child contracts measles infection. The child’s body has to process the antigen & develop B cells & plasma cells that secrete Igs while enduring the disease. The child develops all symptoms of disease but at the same time develops significant Igs for life. OR child can develop active acquired immunity by receiving measles vaccine.. long lasting! - Passive acquired immunity: type of immunity where an individual is given premade, fully formed antibodies against an antigen. Pt is a passive recipient of the antibodies, & their body does not have to perform the actions needed to develop immunity. Provides immediate immunity, but short term.
a.\Ex: when an infant is breastfed & receives fully formed maternally produced antibodies in breast milk OR pt has hep B infection so family member gets administration of HBIg against hep b … short term immunity!
which immunoglobulin is most prevalent?
IgG is most abundant
which immunoglobulin protects mucous membranes of genitourinary, gastrointestinal & pulmonary systems. Activity not related to infection; has protective & preventative role. Found in body secretions (breast milk, tears, sweat, saliva)
IgA
which immunoglobulin binds antigens to B cells. Binds to basophils and mast cells in hypersensitivity reactions. Early stage, when antigen has first entered the body. (location: attached to surface of B cells, in skin, digestive, respiratory tracts)
IgD
which immunoglobulin is abundant in skin, mucous membranes, and respiratory tract. active in allergic reactions; binds to mast cells & basophils to release histamine & leukotrienes. Not related to infection, found in persons with allergies. Type 1 Hypersensitivity reaction. (location: found on mast cells in pulmonary & gastrointestinal tracts) (pollen, dust, animal dander)
IgE
which immunoglobulin initiates complement activity & further immune responses, early infection, RESPONDS FIRST (shows recent/current infection) in infection (location: throughout blood stream) also called macroglobulin due to large size. Forms natural antibodies like ABO blood groups.
IgM
which immunoglobulin activates complement to release inflammatory & bactericidal mediators, confers long-term immunity, active against viruses, bacteria, antitoxins; moves across maternal-fetal barrier. SECONDARY RESPONDER in infection (shows previous exposure)! Late disease, recovery, & long term after, most abundant in bloodstream, most important antipathogenic immunoglobulin in infections & commonly involved in autoimmune disease
IgG
3 stages of HIV
acute HIV infection, chronic HIV infection, AIDS
who is at greater risk for HIV?
African Americans, gay/bisexual men, IV drug users
what happens with HIV is left untreated?
it can advance to AIDS
what shows progression in HIV?
depletion of CD4 T cells.
when is AIDS reached?
when CD4 T cells get to 200 or below and they have a presence of an opportunistic infection such as Kaposi’s sarcoma, TB, pneumocystitis pneumonia, candida infection (thrush), toxoplasmosis, cryptococcus
s/s of AIDS
s/s include headaches, fever, fatigue, rash, weight loss, diarrhea, swollen lymphs, sore throat, muscle/joint pain
Grows slowly, well differentiated, non-invasive, can’t metastasize
benign
Grows quickly poorly differentiated, invasive, can metastasize
malignant
significant risk factor for cancer
Elderly b/c aging allows more time for damage in the cells to build up. They lose telomerase (protective cap) over time
why do malignant cells metastasize
decreased cell to cell adhesion which increases motility of tumor cells. Other changes such as cellular proliferation, angiogenesis (new blood capillaries , increases blood flow ..good purpose: prevent MI, bad purpose would be support cancer cells!), digestion of capsules & barriers by lytic enzymes will cause spreading and metastasis as well.
collapse of a small number of alveoli resulting in reduced gas exchange.
aka collapsed alveoli due to pressure placed on it by fluid. Leads to PNA.
Atelectasis
who is at risk for TB?
People in prison, homeless shelters, schools, third world countries, HIV, people who are immunocompromised
small cell vs non-small cell lung cancer
non-small cell cancer: peripheral location of lungs
small cell cancer: central location of lungs, more aggressive. Already metastasized to other areas of body. most common site = bone, liver, adrenal glands, brain, spinal cord.
this is buildup of fluid in the lungs, due to CHF (left sided heart failure) and ARDS aka Acute respiratory distress syndrome
pulmonary edema
s/s of asthma
Wheezing is number 1 symptom.
cough, dyspnea, maybe use of accessory muscles. DIMINISHED BREATH SOUNDS. Pt could have orthopnea.
this is a bronchoconstriction/inflammatory response so we give steroids to reduce inflammation for this
asthma
a lung condition that causes shortness of breath (dyspnea). The air sacs in the lungs (alveoli) are damaged. Over time, the inner walls of the air sacs weaken & rupture. Obstruction to expiratory airflow, loss of elastic recoil of the alveoli, & high residual volume of CO2 in lung
Emphysema
also known as pink puffer, well oxygenated until later in disease & exhibit pursed lip breathing
emphysema
also known as blue bloater, happens due to hypoxia & cyanosis as well as edema that occurs due to RV failure
chronic bronchitis
this is RV failure caused by pulmonary disease, signs/symptoms include JVD, ascites (fluid collects in abdomen), hepatomegaly, jaundice dyspnea, wheezing, ankle edema, might have 3rd heart sound
cor pulmonale
collapsed lung, air in plural cavity that causes collapse of lung. can be caused by trauma or rupture of alveoli
absent breath sounds UNILATERALLY
pneumothorax
Syndrome characterized by severe and rapid onset of dyspnea, tachypnea, hypoxemia, pulmonary edema, and pulmonary infiltrates
ARDS (Acute respiratory distress)
worsening LV HF leads to …
pulmonary edema
Right ventricular failure and enlargement, commonly seen in chronic emphysema
cor pulmonale
period of seroconversion (HIV/AIDS)
2 weeks to 6 months
sign of lung cancer
hemoptysis
Macrophages contain these substances which allow them to recognize self from non self
MHC (major histocompatibility complexes)
cause of VQ mismatch in PE
decreased blood flow through pulmonary arteries
this leads to pulmonary edema aka backup of blood flow into lungs, s/s include rails, rhonchi, crackles, decreased O2, tachypnea, chronic hypertension, wearing of left ventricular pump, puffy extremities
left ventricular failure
leads to cor pulmonale aka back up of systemic blood flow, s/s include JVD, jaundice, ascites, enlarged liver
right ventricular failure
what are the 5 stages of infectious disease?
- incubation stage (microorganisms being replication without symptoms)
- prodromal stage (symptoms start, often vague/general)
- acute stage (full infectious disease, signs/symptoms in full force trying to fight it off)
- convalescent stage (body starts to eliminate the pathogen, no longer infectious)
- resolution stage (pathogen eliminated)
this is an extension or sign of severe right ventricular heart failure… goes hand in hand with ppl with chronic emphysema & choric bronchitis. This is a back up of blood into venous systemic system including hepatic vein.
cor pulmonale
Serum blood values obtained through arterial blood. Identified alterations in acid-base balance caused by respiratory issues.
ABG (arterial blood gases)
normal ABG values (pH, PCO2, HCO3-, PO2, % Hgb sat)
pH: 7.35 - 7.45
PCO2: 35 - 45
HCO3-: 22 - 26
PO2: 90 - 100
% Hgb sat: 95 - 100
what is the 1st sign of someone in respiratory acidosis?
CNS depression aka change in mental status (remember hypoventilation leads to hypercapnia which leads to respiratory acidosis)
hypoventilation leads to what?
hypercapnia (holding onto too much CO2) which leads to respiratory acidosis (these people are blowers aka trying to blow the CO2 off)
hyperventilation leads to what?
hypocapnia ( getting rid to too much CO2) which can cause alkalosis & CNS excitation
if VQ is unequal, there is an imbalance and a VQ scan should for ordered for what?
pulmonary embolism
no perfusion so PE, weak heart, insufficient blood & hemoglobin, recent MI or heart failure … this will lead to what?
VQ mismatch
ventilate with ______, perfuse with _______
ventilate with air, perfuse with blood
what innervates the diaphragm?
phrenic nerve
C shaped, smaller, less likely to get PNA
left lobe of lung
if this malfunctions, you cough when drinking. this allows you to breathe and drink when you want.
Epiglottis
which type of hypersensitivity reaction is type IV?
Delayed Hypersensitivity
which type of hypersensitivity reaction is type III?
Immune Complex Disorders
which type of hypersensitivity reaction is type II?
Cytotoxic Hypersensitivity
which type of hypersensitivity reaction is type I?
Immediate hypersensitivity
immune responses that is our skin, mucus membranes, enzymes
innate immune response
immune response that once it has seen an antigen, it recognizes it & adapts to it to know how to deal with it next time. Ex: immunizations
adaptive immune response
disorder of acute renal failure, s/s include fever, diarrhea, n/v, stomach cramps, flatulence, stool may have blood/mucus/pus. rare instances kids can have seizures. This can happen from a GI bacterial infection like shigella or E. coli
HUS (hemolytic uremic syndrome)
what type of hypersensitivity reaction is initiated by T lymphocytes that have had previous exposure to an antigen. The T lymphocytes are sensitized to the antigen do not attack the antigen until days after initial exposure. Most common is contact dermatitis. Ex: poison ivy but don’t get itchy til days after exposure. PPD skin test as well. Also occurs in transplant rejection (don’t know til days after)
type IV: delayed hypersensitivity
what type of hypersensitivity reaction occurs when antigen combines with Ig within circulation & these complexes are then deposited in tissues causing organ dysfunction. Autoimmune disease – failing to recognize self. Ex: systemic lupus erythematosus (SLE) where complexes are deposited in kidney, blood vessels, lung skin. Can also be localized such as joints in RA.
Type III: Immune Complex Disorders
which type of hypersensitivity is mediated by Igs directed toward antigens present on cell surfaces. Antibody mediated cell destruction & phagocytosis occur in these reactions. Ex: blood transfusion reaction in which cells from an incompatible donor react with host Igs. Or certain drug reactions.
Type II: Cytotoxic Hypersensitivity
which type of hypersensitivity is an allergy or atopic disorder, rapidly developing immune reaction that occurs after IgE binds to mast cells and combines with antigen, occurs in individuals previously exposed to antigen, local (hives/rash aka urticaria) or systemic. Allergic rhinitis reactions. Can lead to anaphylactic reaction. Ex: pollen, dust, shellfish, peanuts
Type 1: Immediate hypersensitivity
autoimmune disease that is chronic autoimmune inflammatory disorder that affects the joints bilaterally (joint pain/inflammation)
RA (Rheumatoid Arthritis)
What is the transition period?
when your tests show positive and will have flu like symptoms
What is the latent stage or latency period?
when you have it but appear healthy, you aren contagious at this time & don’t know. Most dangerous latent stage of HIV is 2 weeks to 6 months after contraction of virus where bloodwork looks normal, asymptomatic.
what type of vaccine should immunocompromised people never get?
live virus vaccines! because could mutate into disease causing strain
what type of vaccine has the potential, although rare, to mutate into disease-causing strain?
live virus vaccines
enzyme whose function is to regulate BP and filtration rate of the glomerulus
renin
chronic chest pain that the pt has experienced in the past & feels similar to past episodes
stable angina
a cardiac isoenzyme released & increased from dead myocardial cells
CPK-MB (creatine phosphokinase muscle/brain
chronic inflammatory disease affecting the arterial wall that’s caused by agents that damage the endothelial cells
Plaque build up on arterial wall
atherosclerosis
the heart’s pumping action is restricted because of an accumulation of fluid surrounding it
tamponade
pacemaker other than SA or AV node is initiating a contraction: ventricles are beating independently
premature ventricular contractions (PVCs)
chest pain occurring for the first time or is unlike prior episodes; not relieved by rest
unstable angina
s/s of acute MI aka acute coronary syndrome (ACS)
-diaphoresis
-dyspnea
-extreme anxiety
-Levine’s sign (fist to chest)
-pallor
-crushing chest pain that radiates to shoulder, left arm, jaw or back
-weak pulses
this is when chest pain occurs for the first time
unstable angina
this is when a pt has chest pain at rest, caused by coronary artery vasospasm, can be associated w/ MI, life threatening ventricular arrhythmias, sudden death
prinzmetal’s angina aka vasospastic angina
this is a squeezing pain in the chest that occurs when there is a lack of blood flow to the myocardium
angina
this is the hardening & narrowing of the arteries, plaque builds on the arterial walls & restricts blood flow
arteriosclerosis
what is RAAS? & how does it work
-Renin-angiotensin-aldosterone system (RAAS) is a key part of BP regulation
-RAAS is a multistep reaction that raises bp in response to diminished circulation in the body.
It works by:
-when bp is diminished, the kidney is sensitive to the drop in bp so renin (enzyme released by juxtaglomerular apparatus of nephrons in response to decreased perfusion) is released into blood stream stimulating the liver to release large protein aka angiotensinogen.
-In the lungs, angiotensinogen is transformed into angiotensin I then angiotensin converting enzyme (ACE) changes angiotensin I into angiotensin II which is an arterial vasoconstrictor which stimulates the adrenal gland (and raises bp) to release the hormone aldosterone.
-aldosterone works at the nephron to increase Na & H2O reabsorption into bloodstream & secrete potassium into nephron tubules. Retention of Na & H2O increases volume of bloodstream and bp!
low density lipoprotein, deposited on artery walls
what level should it be?
LDL (lousy!!!!!)
less than 130
high density lipoprotein, type of cholesterol that is excreted
**cardioprotective because it carries cholesterol away from the artery walls to be excreted
What level should it be?
HDLs should be greater than 60
this lab is elevated during acute heart failure
BNP (B-type natriuretic peptide)
this causes back flow from one chamber to another
regurgitation
pts w/ hepatic encephalopathy (change in mental status/confusion) will exhibit elevated levels for this lab
ammonia
this is the pacemaker of the heart
SA node
this lab indicates death to myocardial muscle cells
troponin level
most common risk factor for diverticulosis
low fiber diet
one cause of HF due to uncontrolled hypertension causing an enlarged and weakened heart
LVH (left ventricular hypertrophy)
**systolic = life sided HF
these labs will be elevated in pts w/ acute pancreatitis
amylase & lipase
***Increased serum lactic dehydrogenase & C-reactive protein are indicative of severe panc
common sign of diverticulitis
LLQ pain
what is portal HTN and who does it occur in
increased pressure within the portal venous system
occurs in alcoholics, pt w/ cirrhosis & ascites
dyspnea and cough is a s/s of what type of heart failure
LV failure
rhythm disorder in which ventricles beating independently without signal from SA or AV node
aka extra heartbeats
PVCs (Premature ventricular contractions)
pain in BLE w/ activity that improves with rest
intermittent claudication
what is volvulus
what is volvulus
an ejection fraction of what % is indicative of HF?
less than 40%
what are the 3 layers of an arterial wall
- tunica adventitia (connective tissue, outer layer)
- tunica media (smooth muscle, middle layer, expands to accommodate pressure)
- tunica intima (interior lining of artery made of basement membrane & endothelial cells)
what is prostacyclin vs thromboxane A2
prostacyclin = clot formation
thromboxane A2 = clot prevention
this activates clotting
von Willebrand factor
laminar vs turbulent blood flow
laminar = smooth flow parallel to vessel
turbulent = rough flow perpendicular to vessel
s/s of atherosclerosis
only symptom is weak pulse and bruits
Weakened segment of the artery that creates an outpouching that is susceptible to rupture & can cause turbulent blood flow within the artery which causes bulging of walls or dilation (enlarging of the walls)
aneurysm
a true one of these involves all three layers of vessel wall
true aneurysm
what is a false aneurysm
hematoma where the clot is outside arterial wall
s/s of aneurysm
n/v in AAA
no signs if cerebral aneurysm
sudden severe headache then mental status change
subarachnoid hemorrhage (aneurysm)
classic ECG changes with MI
-T wave inversion
-ST Segment elevation
-Q wave development
biochemical markers w/ MI
-elevation of Troponin & T
-increase in CPK-MB (creatinine phosphokinase)
myalgia = muscles aches/pain
arthralgia = joint pain
myalgia vs arthralgia
s/s of Vfib (ventricular fibrillation)
loss of consciousness , death may occur because this is life threatening!
contraction is uncoordinated with no effective pumping during this. you have to shock pt to reset the heart if this occurs
Vfib (ventricular fibrillation)
amt of blood in heart at end of diastole, causes stretch & increased pressure in ventricular chamber increasing SV
preload
amt of resistance the ventricle overcomes to pump blood out of heart
increased this reduces cardiac output
afterload
this is the volume of blood pumped w/ each ventricular contraction
this should be 60-70% in healthy ppl, if under 40% then HF!
LVEF (left ventricular ejection fraction)
cor pulmonale (an enlarged right ventricle in your heart that happens because of a lung condition
right sided heart failure
LVF vs RVF (right ventricular failure)
LVF: affects breathing (dyspnea, cough, orthopnea, PND, weak pulse, decreased cerebral perfusion)
RVF: affects gut (JVD, ascites, GI disturbances, hepatomegaly, splenomegaly, peripheral edema, hepatojugular reflex)
this might develop in HF due to constant aldosterone
hypokalemia (low K)
this is severe RVF which leads to massive peripheral edema, affects most of tissues of body
it is edema w/ fluid leakage after you move your finger print
anasarca
if this is elevated, then indicative of HF
BNP
adverse effects of this is hyperkalemia, angioedema, cough … this treats HF
ACE inhibitors
this has negative side effects that require careful monitoring, med for HF
inotropic drugs
these have a hypotensive effect if combined w/ sildenafil meds
nitrates
s/s of mitral stenosis
dyspnea w/ exertion, PND (paroxysmal nocturnal dyspnea), orthopnea
s/s of mitral insufficiency aka regurgitation
-chest pain (decreased coronary flow)
-pulmonary symptoms due to fluid backup in lungs
-Afib
-diminished S1 sound bc leaflets don’t close
this is intermittent episodes of mild mitral insufficiency, often asymptomatic, can be part of Barlow’s disease aka floppy heart valve syndrome
MVP (mitral valve prolapse)
____________ is a stable virus spread by blood products, bodily fluids, or sexual contact
Hep B
______ is transmitted via blood as in intravenous drug use, sexual transmission is not as likely
Hep C
____ is transmitted via ingestion of contaminated food/water or contracted by unsanitary conditions from person-to-person
Hep A
how to treat inflammation of the esophagus
-Proton pump inhibitor (PPI)
-Histamine-2 blocker (H2 blocker)
What condition is considered to be pre-cancerous and requires frequent evaluation?
Barrett’s Esophagus which results from GERD
what does stool w/ melena look like? (s/s of chronic upper gastrointestinal bleed)
black & tarry
night blindness is associated with what disease
celiac dz due to lack of vitamin A
what causes SBO?
-post op adhesions
-malignancy
-chron’s
-hernia
classic triad for peritonitis (inflammation of peritoneum due to bacterial infection or leakage of intestinal content into peritoneal cavity)
abd pain, abd rigidity, rebound tenderness
IBS (irritable bowel syndrome) vs IBD (inflammatory bowel disease)
IBS- no pathological changes within interior of bowel
IBD- pathological changes in colon (crohn’s dz, ulcerative colitis)
SBO vs LBO
SBO- n/v
LBO- constipation, abd distention
diverticulosis vs diverticulitis
diverticulosis: weakened area bowel wall, small outpouchings that collect intestinal contents & form obstruction
diverticulitis: diverticula inflammation
what lab shows perforation of the bowel or organ
elevated serum amylase
Crohn’s disease vs ulcerative colitis
Crohn’s disease: entire GI wall aka transmural (any part of GI), cobblestones, malabsorption
ulcerative colitis: not transmural (only mucosal layer of large intestine), more common, pseudopolyps, precancerous
unconjugated vs conjugated bilirubin
unconjugated: indirect bilirubin
conjugated bilirubin: direct bilirubin (this is where bilirubin becomes water soluble)
bilirubin is derived from what?
the breakdown of aged RBCs
pts w/ liver dysfunction are at increased risk for what?
blood clots
what causes jaundice
excessive RBC hemolysis (too much breakdown/destruction), hepatocellular injury, bile duct obstruction
this occurs when the liver may not be secreting bile for fat digestion
steatorrhea
which hepatitis is contaminated food/water and fecal oral
Hep A (HAV)
bc A for agriculture aka food
and bc A & E come from the sea aka water
if it ends w/ a vowel then it comes from the bowel!
which hepatitis(s) is blood/body fluids
Hep B (HBV)
Hep C (HCV)
Hep D (HDV)
which hepatitis is contaminated water and fecal/oral route
Hep E (HEV)
bc A & E come from the sea aka water.. if it ends w/ a vowel then it comes from the bowel!
this disease is silent & gradual, irreversible damage due to collagen & connective tissue infiltration … #1 caused by HCV then alcoholic liver disease, NAFLD
**9th leading cause of death in US
cirrhosis
ppl with this hepatitis can still be carriers of this inactive hepatitis
Hep B (HBV)
this hepatitis is the #1 cause of cirrhosis
Hep C (HCV)
risk factors for chronic pancreatitis
-30 to 40y/o
-AA
-alcohol induced in men, lipid induced in women
-genetics if under 30
what labs will be elevated for pancreatitis
amylase & lipase !!!
CBC, glucose, CRP as well
jaundice may be the first sign of this cancer due to tumor compromising bile duct
pancreatic cancer
s/s of PAD (peripheral arterial disease)
pulseless
pallor
cold
hairloss
smooth, shiny skin
ulcers
2nd leading cause of death resulting from cancer, preventable disease
colorectal cancer
the alternate or “backup” blood vessels in your body that can take over when another artery or vein becomes blocked or damaged.
collateral circulation
these divide into right and left bundles that fire rapidly to allow for simultaneous excitation of the right and left ventricles
purkinje fibers (aka subendocardial branches)
this travels down the septum between the ventricles and purkinje fibers in the walls of both ventricles
also called atrioventricular bundle
bundle of HIS
s/s of pulmonary edema
s/s: rails, rhonchi, crackles, decreased O2, tachypnea, chronic hypertension, wearing of left ventricular pump, puffy extremities
this is a major cause of heart valve disorder. It starts off as an acute streptococcal throat infection and turns into this
what happens when left untreated?
Rheumatic fever
If left untreated, pt will suffer valvular dysfunction and have rheumatic heart disease, an inflammatory condition of the heart and heart valves. BUT this should easily be treated w/ antibiotics.
ulcerative colitis vs Chrons disease
UC = autoimmune, erosions in mucosal layer coalesce into ulcers, edema, abscesses. s/s include bleeding, cramping, urge to defecate, necrosis can occur, diarrhea, blood stool w/ pus.
s/s = bleeding, cramping, urge to defecate, necrosis can occur, diarrhea, blood stool w/ pus
Chron’s Disease = autoimmune, inflammation spreads through submucosa to deeper layers of intestinal wall. s/s include malabsorption, weight loss, Steatorrhea (oily/fatty stool)
s/s = malabsorption, weight loss, Steatorrhea (oily/fatty stool)
bleeding, cramping, urge to defecate, necrosis can occur, diarrhea, blood stool w/ pus
s/s of ulcerative colitis
malabsorption, weight loss, Steatorrhea (oily/fatty stool)
s/s of Chron’s disease
pH 7.50, PCO2 50, PO2 85, HCO3 35, SaO2 95
metabolic alkalosis
burns, crush injury, CKD, CHF, ACE, ARB, NSAID use
hyperkalemia
common cause of metabolic acidosis
DKA (Diabetic ketoacidosis)
CKD, DKA, burns, diarrhea, vomiting, fever dehydration, DI (diabetes insipidus), increased dietary intake
hypernatremia
(bc increased dietary intake & diarrhea are key words)
buildup of nitrogenesis waste in the blood
azotemia
neurotransmitter decreased inmysento gravis
acetylcholine (ACH)
electrolyte abnormality causes muscle spasms, cramps, paresthesia
hypocalcemia
signs of waste build up in the blood stream
uremia
pH 7.50 pCO2 55 PO2 55 HCO3 31 SaO2 92
metabolic alkalosis
physical signs of compensation for metabolic acidosis
hyperventilation - rapid & deep respirations
priority system to assess w/ potassium abnormality
cardiovascular system
NSAIDs, CKD, diuretics, CHF, increased water intake can cause abnormalities w/ this electrolyte
Hyponatremia
excessive sweating, vomiting, diarrhea, diuretics, poor dietary intake, CKD, alcoholism are risk factors for this electrolyte abnormality
hypokalemia
risk factors for respiratory acidosis
spinal cord, brain injury, opioids/narcotics bc reduced RR
what provides collateral circulation to the brain
Circle of Willis
(good & bad things; bad thing is most common site of aneurism)
this is inactive if you have poor renal function which can cause what
Vit D
which can cause hypocalcemia
Normal BUN (Blood Urea Nitrogen level)
& what can affect BUN level?
5-20 mg/dL
BUN can be high or low based on hydration status (look at gravity – it tells you dehydration)
Can be seen in those with extremely muscular individuals (athletes) and high protein diets bc of high muscle breakdown. Muscle cell proteins break down into amino acids which are nitrogen compounds.
low albumin means low this
low protein
this it the destruction of RBCs
in CRF- it is not regulating RBC production
hemolysis
this is a complication in CRF that is confusion, coma, death
Encephalopathy
isotonic vs hypertonic vs hypotonic solutions
isotonic: NS 0.9% saline, Lactated ringers (temporary replacement for blood)
hypertonic: 3% NaCl, ICF to ECF so cells shrink. This is more rare bc it’s dangerous to use. Used in ICU or surgery sometimes. Used for cerebral edema (swelling in brain)
hypotonic: 0.45% NaCl, (ECF to ICF to treat dehydration. Causing cells to enlarge)
dehydration causes this
Decreased circulating blood volume leads to tachycardia and hypotension
s/s of respiratory alkalosis
anxiety
restlessness
pain
CNS excitation
increased VS
normal or decreased BP
cardiac problems
electrolyte imbalances
s/s of respiratory acidosis
CNS depression
respiratory distress
decreased BP but increased VS
Increased respirations, tachycardia, hypotension, confusion
metabolic acidosis
Confusion, dizziness, weakness, diarrhea
metabolic alkalosis
pt has severe asthma, what is going on ?
respiratory acidosis is occurring … so pt will hyperventilate (respiratory alkalosis will happen!) to compensate
Cushing’s triad is a sign of increased ICP. What does it consist of?
Hypertension, Widened pulse pressure, Bradycardia,
Abnormal respiratory pattern
This causes a thunderclap headache (comes out of nowhere, most severe headache that causes n/v even seizure, stiff neck, etc)
SAH (Subarachnoid hemorrhage) = brain bleed
hypovolemeia vs hypervolemia
& causes!
hypovolemia = condition that occurs when your body loses fluid, like blood or water. (dehydration is a cause)
hypervolemia = too much fluid in your body
(heart failure, kidney failure, cirrhosis causes this)
ABGs
- Respiratory Acidosis (caused by respiratory disorders, and most CNS disorders like head injuries, drug OD): s/s include respiratory distress/working hard to breathe, headache, fatigue, SOB, rapid breathing, cough, restlessness, anxiety, confusion.
- Respiratory Alkalosis (caused by Pain/Anxiety/Labor, certain drugs, early hypoxia which leads to increased RR to get in more CO2, resulting in loss of too much CO2): s/s include anxiety, dizziness, confusion, tachycardia, palpitations, hypotension, pain, muscle cramps
- Metabolic Acidosis (caused by DKA, diarrhea, kidney failure): s/s include dysrhythmia, anorexia, hypotension, sleepiness, lethargy, confusion, coma, headache, seizures.
- Metabolic Alkalosis (caused by Vomiting, NG suctioning, too much antacid tx, hypokalemia, diuretics): s/s include confusion, dizziness, agitation, weakness, vomiting, diarrhea, seizures
this is an autoimmune neuromuscular disorder that can occur at any age.
***ptosis is the first sign!
Caused by loss of ACH receptors in neuromuscular junction
**s/s: muscle weakness and fatigue
Myasthenia gravis
2 most common causes of CRF
Atherosclerosis (plaque buildup of fats, cholesterol/other substances in & on the artery walls that causes arteries to narrow which blocks blood flow and can cause clots)
and diabetes are the most common causes of CRF in older adults
complications of CRF
Cardiovascular disease (heart disease and/or stroke), high b/p, anemia, metabolic acidosis, gout
kidney disorder that causes body to pass too much protein in your urine (proteinuria).
why does it occur
nephrosis , occurs due to damage to the clusters of small blood vessels in kidneys that filter waste and excess water from blood.
this is central & leads to decreased ADH production, causing decreased water retention by the kidneys; can be caused by brain tumor, surgery, or infection. Blood volume and electrolytes are decreased.
s/s: thirst, polyuria, hypernatremia, dilute urine
DI (Neurogenic Diabetes Insipidus)
excessive growth hormone stimulates a gradual growth of certain bones such as jaw, hands, feet, & overactive sweat glands are characteristic features (Andre the Giant!)
Acromegaly
what problems should be monitored for when it comes to acromegaly? aka excessive growth hormone
hypertrophy of organs , insulin resistance, increased risk of colon polyps, pressure of pituitary tumor against brain tissue causing headaches and visual impairment
Most common cause = ectopically produced ADH associated with cancer. (esp. small cell carcinoma of the lung)
Characterized by high levels of ADH; this increase causes hyponatremia & concentrated urine
SIADH (Syndrome of Inappropriate Antidiuretic Hormone)
Hashimoto’s vs Cretinism
Hashimoto’s – chronic autoimmune thyroiditis that is most common cause of hypothyroidism, iodine sufficiency
Cretinism – result of thyroid hormone deficiency during embryonic development and early neonatal life. Child exhibits short stature, intellectual disability, & other metabolic disorders
Most common cause of hyperthyroidism, an autoimmune stimulation of the thyroid gland.
s/s include slight tremor of the hands or fingers, heat sensitivity, weight loss, an enlarged thyroid gland, bulging eyes, thick, red skin on the shins or feet, menstrual cycle changes, problems getting an erection, low sex drive, and fast or irregular heartbeat.
Grave’s Disease
thyroid storm, overwhelming release of thyroid hormones that exerts an intense stimulus on the metabolism. (due to hyperthyroidism)
what is this and the s/s of it?
Thyrotoxic crisis
Medical emergency, heart failure & pulmonary edema can develop rapidly & cause death.
**s/s = high fever, tachycardia, n/v, tremulousness, agitation, psychosis.
This is caused by trauma or inadvertent damage or removal of the parathyroid glands during thyroid surgery.
s/s include muscle cramps, irritability, tetany, convulsions
hypoparathyroidism
this is also known as hyperadrenalism or hypercortisolism which is an endocrine disorder caused by high levels of cortisol in the blood.
Cushing’s syndrome
T1 vs T2 DM
Type 1: insulin dependent, mostly developed in children. Three Ps: Polyphagia (cells starve leading to hunger), polyuria (excessive urine output), polydipsia (increased thirst)
Type 2: insulin resistance that’s developed later on. Can cause recurring infections, poor wound healing.
s/s of hypoglycemia (low blood sugar)
anxiety, tachycardia, sweating, cold/clammy skin, pallor, confusion, crying slurred speech, paresthesia, ataxia, lethargy, sleepiness, coma, possible death if severe
DKA vs HHS (Hyperosmolar hyperglycemic state)
DKA = type 1 diabetics, Ketones that are produced are flushed out by polyuria (excessive peeing) and also out through their breath (fruity)
o s/s include dehydration, n/v, lethargy, decreased LOC, fruity odor, ketonuria, glucose levels 300-750mg/dL
*HHS = Hyperosmolar hyperglycemic state, does not involve ketones like DKA, usually in type 2
o s/s include extreme thirst, frequent urination, confusion
sign of diabetic nephropathy?
Microalbuminuria (protein in urine)
patients always present with this if diagnosed w/ acute leukemia
radiation exposure
measures the number of new RBCs in the blood and helps determine whether the bone marrow is producing new red blood cells at an appropriate rate.
Reticulocyte
bone marrow makes excessive amounts of RBCs.
Polycythemia
lack of vitamin B12 which results in the inability of the body to make enough mature RBCs and allows breakdown of the myelin sheaths surrounding some of the body’s sensory and motor nerves.
pernicious anemia
excess of all blood cell types (RBCs, WBCs, platelets) in bone marrow
Polycythemia vera
thrombocytopenia vs Thrombocytosis?
Thrombocytosis = excessive number of platelets which can cause clotting, more than 750,000/uL
Thrombocytopenia = low number of platelets, fewer than 100,000/uL
2 forms of bone
- Cortical bone- solid, dense
- Trabecular / cancellous bone- nonsolid, composed of meshwork that makes the bone porous.
4 types of bone cells
1.Osteoblasts: bone forming cells that secrete osteoid, which forms the bone matrix. They begin mineralization and are unable to divide.
2.Osteocytes: mature osteoblasts that maintain metabolism and nutrient and waste exchange; they are unable to divide.
3.Osteoclasts: function in resorption and degradation of existing bone, the opposite of osteoblasts.
4.Osteoprogenitor cells: immature cells that differentiate into osteoblasts. They divide.
5 stages of bone healing
- Fracture & Inflammatory phase: 1st phase of bone healing, bleeding initially occurs between the edges of fractured bone, and a hematoma develops during first few hours and days. Inflammation causes vascular permeability & the attraction of WBCs. This phase peaks ~48 hours after injury and can last up to a week.
- Granulation tissue formation: fibroblasts are attracted to the area of injury, there is a growth of vascular tissue. Nutrient & oxygen supply during this early process is significant. This stage lasts ~2 weeks.
- Callus formation: callus if formed which is osteoblasts and chondroblasts in granulation tissue. These cells synthesize the extracellular organic matrix of woven bone & cartilage, producing new formed mineralized bone ~6 weeks postinjury.
- Lamellar bone deposition: 4th phase of bone healing, strengthening phase where ossification begins. Meshlike callus of woven bone is replaced by sheets (lamellae) or mineralized bone that are organized parallel to the axis of bone & mechanically stronger than the bone of a callus. The length of time of this phase depends on the injury; occurs in weeks following callus formation.
- Remodeling: final phase, remodeling of the bone at site of healing fracture by osteoblasts & osteoclasts. Formation is sculpted and refined by mechanical stresses imposed on the bone. Adequate strength commonly occurs in 3-6 months.
This occurs when tissue pressure exceeds perfusion pressure in a closed anatomical space. Compartments are groups of muscles, nerves, and blood vessels within a space that’s contained by a tough fascial membrane. Fascial membrane can’t accommodate swelling/bleeding in compartment space due to inflexible.
Signs/Symptoms include pain that is out of proportion to the degree of the injury, decreased or absent pulses distal to the injured region, sensory loss/paresthesia distal to injury, pallor, decreased cap refill.
compartment syndrome
2 types of delayed union (fracture that’s taking more time than normal to heal)
- Malunion – healing of bone in an unacceptable position
- Nonunion – permanent failure of healing of bone
this is a broken bone caused by disease, often by the spread of cancer to the bone.
pathological fracture
Infection of the bone caused by a microorganism, most commonly a bacteria.
osteomyelitis
who is at risk for hip fxs
Older age, being female, European American females
2 types of rotator cuff injuries
- tears of the tendons & muscles
- tendonitis which is inflammation of the tendons. These occur mostly due to sports injuries causing constant shoulder rotation like baseball pitching or swimming.
what causes tendonitis
strain, overuse, injury, or too much exercise. Tendonitis may also be related to a disease such as diabetes, rheumatoid arthritis, or infection.
OA vs RA
Osteoarthritis – degeneration of joints caused by aging; the joints of the hands and knees are particularly affected. RF: - aging, fam hx, obesity, overuse of joints
Rheumatoid arthritis – chronic autoimmune inflammatory disorder that affects joints and may have systemic effects. RF: fam hx, smoking, possible viral illness
this is a disorder of recurrent inflammation trigged by hyperuricemia (elevated uric acid in blood and high uric acid crystals in the synovial fluid)
gout aka gouty arthritis
complications of gout
uric acid crystals become deposited in subcutaneous tissue surrounding joints, termed tophi (tophus is a palpable, subdermal, hard nodule commonly visible in the Achilles tendon, joints of hands, elbows, or pinnae of ears).
Can also develop fever, nephropathy (kidney disease), and nephrolithiasis (stones).
