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316 Cards in this Set
- Front
- Back
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atrophy
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decrease in cell size, any organ
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hypertrophy
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increase in cell size
esp heart an kidney |
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hyperplasia
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increase in # of cells
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dysplasia
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abnormal change in size, shape, organization
-constant cell turnover |
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metaplasia
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reversible replacement of a mature cell by another, usually replacement cell is less differentiated and functional
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atrophy physiologic and pathologic
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phys: losing muscle mass after MVA
path: alzheimer's, cell signaling |
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hypertrophy phys and path ex
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phys: hormonal, work induced: preg
path: hormonal, heart disease, after MI stress increases |
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hyperplasia physiologic and pathologic ex
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phys: response to injury, callus from running
path: endometrium, hormones, preg, high traffic areas |
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ex of metaplasia
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smoker, columnar cells in respiratory tract, their fxn is to use cilia to move but then cells come w/o cilia
-increased risk for bronchitis etc |
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free radicals
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electrically uncharged or group of atoms having an unpaired electron
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free radicals damage...
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1. lipid peroxidation
2. alteration of proteins 3. alteration of DNA 4. mitochondria |
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RAAS System and ROS
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Renin-Angiotensin-Aldosterone System
-potent vasoconstrictors (renin and ang II) -HTN |
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how is ROS related to RAAS, what upregulates ROS
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ang II and renin upregulate ROS
-certain diseases does ROS too |
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cellular response to hypoxia
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-decrease in ATP, Na/K pump fails
-cellular swelling -vacuolation -reperfusion injury |
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compartment syndrome
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swelling in confined area that can't hold it
-Ca is left over the muscle which can't contract,after injury because it deposits from prolonged |
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lead poisoning
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-worse if nutrition is compromised
-affects NS, hematopoietic system, kidneys -ability to interfere w/ fxns of Ca and can increase it intracellularly |
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carbon monoxide
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higher affinity for Hb
-O2 deprivation -headache, giddy, tinnitus, nausea, weakness, vomit |
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total body water
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-intracellular fluid: 2/3
-extracellular fluid: interstitial, intravasc, lymph, synovial, CSF etc |
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water and pediatrics
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75-80% of weight
-susceptible to signif change in bodily fluids...DEHYDRATION |
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aging and TBW
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it decreases (% of fluid)
-more adipose and less muscle -renal decline -thirst perception -decreased thyroid fxn |
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edema
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accumulation of fluid within interstitial spaces (extracellular)
-problem with distribution NOT excess |
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location of edema
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generalized or localized
-ex: fluid on particular organ, DVT w/ diff osmotic pressure, prolonged standing proteins can be culprit, disrupt oncotic P by pulling fluid |
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what determines severity of edema
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pitting, you stink finger and it looks like it's still there
-edema doesnt stop unless you stop it |
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weaping edema
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so much interstitial that it breaks permeability of skin
-serous fluid seeps out -goes to dependent place away from the heart -ex: feet up, edema goes to back/sacrum if laying down |
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thirst and loss of TBW
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2%
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primary ECF cation and what it does
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Na
-regulates osmotic forces -neurotrans -irritability -acid-base balance -cellular chemical rxns -membrane transport |
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regulators of Na
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renin
angiotensin I and II aldosterone |
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more than 5 or 6 g of Na will do what
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increase edema because water follows sodium
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primary ecf anion and hwat it does
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Cl, follows Na
-electroneutrality |
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what thirst does to the blood and the body
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increased osmolarity, viscosity
-or blood vol and BP go down -vol. delpletion condition -ADH secretion increases |
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where is aldosterone from and major fxn
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adrenal cortex
governs sodium -overstim=HTN |
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where is renin made and fxn
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JG cells of kidney
-tubular reabsorption in kidney -increased vasoconstriction |
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hypernatremia value
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> 147 mEq/L
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hypernatremia definition
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-water loss or Na+ gain
-inadequate free water intake -inappropriate admin of hypertonic saline soln -oversecretion of aldosterone, primary hyperaldosteronism |
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cushing syndrome
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high aCTH concentration
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hyponatremia value
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< 135 mEq/L
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hyponatremia
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Na deficits = plasma hypo-osmolarity and cellular swelling (take any H20 you can)
-causes diuretic -N/V -GI suctioning -burns |
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dehydration s/s and solution
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turgor, skin tenting, dry mucous membranes, increased temp
-soln: D5W IV to rehydrate bc saline can pull Na, use sugar not to lyse RBCs |
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what happens when tubular fxn can't concentrate urine, where is this seen
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renal clearance of free water increases
-diabetes insipidis, decreased ADH -MVAs |
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manifestations of water deficits
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thirst
tachycardia weak pulses postural hypotension (brain needs to perfused) elevated hematocrit and Na level |
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water excess is a syndrome of
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inappropriate ADH (SIADH)
-conserving water, severe congestive heart failure, brain trauma -ADH secretion in absence of hypovolemia or hyperosmolarity -Hyponatremia w/ hypervolemia OCD too |
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fxns of potassium in the body
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-regulates intracellular electrical neutrality in relation to Na and H+
-essential for transmission and conduction of nerve impulses, normal cardiac rhythms, skeletal and smooth muscle contractions (resting mem pot) |
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what affects potassium balance
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-changes in pH: if H+ accums in ICF during acidosis the K moves out to balance
-Aldosterone -Insulin -Catecholamines |
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where and how much of potassium is reabsorbed in the body
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90% by the proximal tubules of LOH
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what happens to potassium with high aldosterone levels
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K concentration increases
hyperkalemia -pump stumps working and you use insulin |
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most common type of skin cancer
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basal cell carcinoma
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basal cell carcinoma
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neoplasm of the nonkeratinized cells of the basal layer
-usually a non-metastasizing tumor that extends wide and deep -UVR exposure major factor |
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second most common skin cancer
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squamous cell
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risk factors for squamous cell
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UVR exposure
arsenic coal paraffin |
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two types of squamous cell carcinoma
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1. intraepidermal squamous cell: remains contained for long periods of time but when not contained spreads to lymph
2. invasive: red scaling, keratotic, slightly elevated lesion with irreg borders, looks like outward ulcer |
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metastasis and squamous cell and 5 year survival rate
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seen about 25% of the time with squamous and the 5 year survival rate when met does occur is about 25%
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malignant melanoma
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malignant tumor of melanocytes
-rapid, aggressive tumor and almost always metastatic |
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most affected by malignant melanoma
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blondes and red heads
-prob genetic but definite familial link noted |
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risk assessment for malignant melanoma
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-presence of marked freckling on upper back
-Hx of 3 blistering sunburns before the age of 20 -Presence of rough, dry patches that look like freckles -No particular size or shape -Irregular borders -Uneven surface |
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Criterion of assessment for malignant melanoma
ABCD RULE*** |
Assymetry
Border irregularity Color variegation Diameter greater than 6 mm |
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what level do you want K concentration below?
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5.5 mEq/L
2.5-5 is preferred |
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what happens if the K conc is above 6
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-decrease in QT interval
-prolonged PR interval -widened QRS complex -bradycardia -tall T-waves...die within hour |
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symptoms of hyperkalemia
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NONE
silent killer -lose neuron fxn before death |
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treatment for hyperkalemia
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Calcium glucanate-restores neuromuscular fxn, insulin pump
-NaCO3 -Dialysis -K exelate: enema, drink, bind K and pee/poop fast |
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hyperkalemia mild attacks
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increased neuromuscular irritability
-tingling of lips and fingers -restlessness -intestinal cramping -diarrhea |
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hyperkalemia severe attacks
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-cells can't repolarize
=muscle weakness -lose muscle tone -flaccid paralysis -ECG changes can be life threatening...tombstone T waves |
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where is most of calcium
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99% in bone as hydroxyapatite
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why do you need calcium
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bones
teeth blood clotting hormone secretion cell receptor fxn muscle conduction |
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normal levels of ca
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4.5-5.5 mEq/L
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chvostek sign
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tap facial n at temple area and cheek should come up
chekcing for calcium |
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where is phosphate and why do you need it
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85% in bone
-necessary for high-energy bonds located in creatine phosphate and ATP -ion buffer 2.5-4.5 |
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acids are formed as end products of
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protein cho and lipid metabolism
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major organs involved in pH regulated
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bones
lungs kidneys |
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body acids in 2 forms
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1. volatile: lung, H2Co3...eliminate as Co2, h attach and exhale
2. non-volatile: renal: sulfuric, phosphoric and other organic acids...elim by renal tubules w/ bicarb |
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buffer
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chemical that can bind excessive H or OH without a signif change in pH
-weak acid and conjugate base |
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most important plasma buffering system
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carbonic acid
bicarbonate system hemoglobin KIDNEY but not fastest |
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respiratory acidosis
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elevated pCO2, cant rid Co2
-ventilation depression |
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respiratory alkalosis
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decrease in pCo2 as a result of alveolar hyperventilation
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metabolic acidosis
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decrease of bicarb or increase in noncarbonic acids
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metabolic alkalosis
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increase in bicarb, excess loss of metabolic acid
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characteristics of benign tumors
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-grow slowly
-well defined capsule -non-invasive -well differentiated -low mitotic index -don't metastasize |
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characteristics of malignant tumors
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-grow rapidly
-non-encapsulated -invasive -poorly differentiated -high mitotic index -spreads distantly |
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malignant tumor named by
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tissue from which it arises
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insitu
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cervix, skin, oral cavity, esophagus, bronchus,
-pre-invasive, hasn't broken basement membrane |
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malignant epithelial tumors
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carcinomas
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sarcomas
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malignant CT tumors
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cancer stem cells
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self-renewing
-cell division creates new stem cells -multipotent: able to differentiate into multiple different cell types |
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tumor cell markers
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substances produced by cancer cells or that are found on plasma cell membranes in the blood, CSF, or urine
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prostate specific antigen
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hormones, enzymes, genes, antigens, antibodies
-tumor cell marker |
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cancer causing mutations
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-clonal proliferation or expansion
-as a result of a mutation a cell acquires characteristics that allow it a selective advantage -increased growth rate or decreased apoptosis -multiple mutations are required before it becomes cancer |
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hallmarks of cancer
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-self-sufficiency in growth signals
-insensitivity to antigrowth signals -evading apoptosis -limitless replicative potential -sustained angiogenesis: new cap vessel demand -tissue invasion and metastasis |
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oncogenes
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mutant genes in non-mutant state
-direct protein synthesis and cellular growth |
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tumor suppressor genes
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encode proteins that in their normal state negatively regulate proliferation
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mutation of normal genes
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point change in 1 or a few nucleotide base pairs
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chromosomal translocation
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piece of one chrom transferred to another
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chromosomal amplification
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duplication of a small piece of a chromosome over and over
-beginning of cancer spreading |
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caretaker genes***
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encode for proteins that are involved in repairing damaged DNA
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genetics/cancer-prone families
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mutagen exposure
genetic events but NOT inherited -mutations in tumor suppressor genes |
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implicated viruses and cancer
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hep B and C
-epstein-barr virus -kaposis sarcoma -herpes virus (HPV) -human t-cell leuk-lymphoma |
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bacterial cancer causes
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helicobacter pylori
-chronic infections associated with GERD, peptic ulcer disease, stomach carcinoma, mucosa-assoc lymph |
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inflammation and cancer
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chronically it can cause it
-cytokine release from inflammatory cells, FR's -mutation promotion -decreased DNA damage response |
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phases of tumor spread
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transformation
growth local invasion distant metastasis |
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tumor spread
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direct local invasion of contigous organs
-metastasis by implantation to distant organs...lymph and blood |
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types and ways of tumor spread
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-mechanical: roots
-surgical: not encapsulated -proteases: secreted by malignant tumors and destroy normal tissues -slip: cancer cells slip in between normal cells -increased motility: extravasate |
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staging of cancer
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-involves tumor size
-degree to which it has invaded and spread 1.local 2. locally invasive 3. spread to regional structures like lymph 4. spread to distant sites: liver, bone and lung |
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clinical signs of cancer
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pain
fatigue weight loss...cachexia anemia asthenia altered taste leukopenia,thrombocytopenia paraneoplastic syndromes |
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chemotherapy
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non-selective cytotoxic drugs target vital cellular machinery or metabolism pathways critical to malignant and normal cell growth and replication
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goal of chemo
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eliminate enough tumor cells so body's defense...
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radiation
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contain, reduce, eradicate without excessive toxicity
-avoid damaging normal structures -damages cancer cell DNA |
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endocrine system fxn
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-differentiation of reproductive and CNS in fetus
-stim of growth and development -coordination of male and female reproductive system -maintain internal envt |
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what inactivates hormones
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liver, renders them more water soluble for renal excretion
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why you would have elevated or depressed hormone levels
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-failure of feedback mechanisms
-dysfxn of an endocrine gland -secretory cells are unable to produce, obtain or convert hormone precursors -endo gland synth or releases excessive amts of hormone |
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diabetes insipidus and s/s
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an insufficiency of ADH
**POLYURIA AND POLYDIPSIA |
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3 forms of diabetes insipidis
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1. neurogenic: insufficient ADH caused by some sort of trauma or organic lesion on post pit
2. nephrogenic: usually genetic/acquired, idiopathic, inadequate response to ADH end=organ failure of renal system 3. psychogenic: OCD excessive water intake |
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how to tell diabites insipidis from mellitis
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can't concentrate urine, specific gravity is low
-w/ diabetes mellitus it's very high |
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eval and tx for diabetes insipidis
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-differentiate between DI and DM
-test urine for specific gravity -1-2L is normal -4-8L a day with DI -draw plasma ADH to see if decreased conc of DDAVP, supportive of BP but doesn't cure it -water deprivation test, UO should drop but DI won't |
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chronic DI and DI with head trauma
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chronic: huge bladders and wet kidneys
head: correlate s/s and history |
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SIADH and what dx is based on
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-high levels of ADH in the absence of normal demand on the body
-can be caused by cancers, some tumor cells secrete ADH -Dx is based on whether pt has NL adrenals and thyroid fxn -occassionally psych popn due to vol of psychotropic meds |
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transient siadh
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may follow surgery because stored ADH is released from gland during surgery (5-7 days)
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signs and symptoms of SIADH
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-water overland
-increased TBW -hyponatremia by dilution -plasma hypo-osmolarity with concentrated urine -Edema -CHF, hypovolemia, thirst, anorexia, dyspnea on exertion, fatigue, dull sensations |
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severe SIADH symptoms
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confusion
lethargy convulsions |
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Tx of SIADH
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hypotonic saline and fluid restriction
-no drug treatment to fix tumor secretion of ADH |
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hypopituitarism and s/s
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absence of hormone
-complete failure of fxn -infarct of gland(common hypoxia, stroke, emboli), space lesions s/s: var and depends on which hormones are affected |
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panhypopituitarism
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affects all
-ACTH deficiency and GH -TSH deficiency -FSH and LH deficient |
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hyperpituitarism
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-common from benign, slow-growing lesions
-pituitary adenoma -usually asymptomatic, poses no harm |
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manifestations of hyperpituitarism
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headache and fatigue
visual changes hyposecretion of neighboring anterior pituitary hormone like GH |
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eval and tx of hyperpituitarism
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eval: always MRI for ant pit disease
Tx: transssphenoidal tumor resection -radiation, not best |
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ACTH deficiency
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cortisol deficiency is a result
-need for stress hormone and storage -elevates in DM -can lose weight quickly, - sleep disturbance, weight gain |
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life threatening part of ACTH deficiency
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N/V
anorexia inappropriate CHO metab muscle wasting fatigue weakness |
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hypersecretion of GH****
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acromegaly: ADULTS
gigantism: children and adolescents |
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hyposecretion of GH
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dwarfism
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what is hypersecretion of prolactin caused by and s/s males and females
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-prolactinomas
females: increase causes amenorrhea, galactorrhea, hirsutism, osteopenia males: hypogonadism, ED, impaired libido, oligospermia, decreased ejaculate volume |
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hyperthyroidism and s/s
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(graves disease or thyrotoxicosis)
-LARGE PROTRUDING EYES -results from nodular thyroid disease...Goiter S/S: lower TSH, high TH, tachycardia, heat intolerant, overstim of CNS *thyrotoxic crisis: s/s worsen and CNS you seize etc |
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primary hypothyroidism
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subacute thyroiditis
-non-inflammatory -autoimmune thyroiditis (Hashimoto Disease, leukocytes) -postpartum thyroiditis around 6 mos -myxedema:chronic -coma in older ppl |
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secondary hypothyroidism
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congenital
thyroid carcinoma radioiodine or med exposure |
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hypothyroidism s/s
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slowing of CNS
cold fluid lower TH high TSH |
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primary hyperparathyroidism
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excess PTH
N1 feedback mechanism such as elevated Ca doesn't inhibit PTH secretion -idiopathic |
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secondary hyperparathyroidism
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high PTH, secondary to chronic disease
-renal failure -glomuler filtration=lower vit D and Ca so stim of PTH doesn't stop -intestinal malabsorption of vit d and Ca -ingestion of drugs: Dilantin, chronic laxatives |
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hypoparathyroidism
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usually PT gland damage during surgery
-usually transient -may need Ca and vit D until resolved |
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type I diabetes mellitus...2 types and describe
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-pancreatic atrophy and specific loss of beta cells that secrete insulin
-macrophages, T and B lymphocytes, NKCs here 1. immune: assoc w/ IgG islet cell antibodies, juv onset 2. non-immune |
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fxn of alpha cells of the pancreas
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feedback to liver to make glucose while you sleep
(gluconeogenesis) -convert stored to active |
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type I diabetes
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genetic susceptibility
more common in kids envt factors immunologically mediated destruction of beta cells 5-10% of all cases |
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manifestations of s/s
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-hyperglycemia
-polydipsia -polyuria -polyphagia -weight loss -fatigue |
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types of type 2 diabetes
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maturity onset diabetes of youth
gestational in 3rd tri insulin resistance |
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diabetes mellitus definition
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syndrome of disturbed CHO, lipid and protein metabolism characterized by hyperglycemia that results from a deficient action of insulin on target tissues
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normal blood glucose levels, IFG and DM
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normal: 60-100
IFG: 100-126 DM > 126 |
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type 2 diabetes...tx, % of cases and why the rise
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pills or insulin
90-95% of all, > 19 million -aging popn, dx criteria is evolving -pima native americans -older than 75 makes up majoritty |
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non-modifiable risk factors for diabetes
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-genetics & familial
-ethnicity: blacks, latino, natives -age: pancreas fxn decreases as you get older |
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modifiable risk factors for diabetes
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obesity
physical inactivity elevated fasting and 2h glucose levels diet: high fat and sugar(soda) insulin resistance impaired insulin secretion |
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metabolic defects of type II
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-decreased pancreatic insulin secretion
-peripheral insulin resistance in muscle and fat -increased hepatic glucose output |
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explain peripheral insulin resistance in muscle and fat
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get too much insulin
cell damage and they morph to be more resistant -stores fat |
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explain alpha cell and increased hepatic glucose
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stimulates liver for gluconeogenesis, defective chemical release/signal to liver exclusively
-none, too little or too much can happen |
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explain beta cells, why you need glucose and what happens when its defective
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need for ADP/ATP, K, Ca channels or you have impaired signaling
-defect: very fast and insulin secretion will dump out or not at all |
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biphasic insulin secretion normal
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1. instantaneous: 1-2 min, drops after 10 until you eat more, up to 1 hr, initial insulin dump is huge spike
2. rises gradually until blood sugar drops, don't need it and it shuts off -several min to hours -derived from stored secretory granules & de novo insulin synthesis -persists as long as glucose is elevated |
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biphasic insulin secretion with a diabetic
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1st-smaller release, not a huge dump
-derived from stored secretory granules 2nd-smaller, doesn't get sustained -can look erratic, close to normal or episodic |
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type II diabetes morphology
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amyloid plaques settle into pancreas
-delta cells with somatostatin |
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normal beta cell characteristics
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-majority of pancreas
-produce insulin and amylin -amylin helps glucose uptake, drug target may help cell signaling -insulin in response to elevated blood glucose |
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normal alpha cells
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-periphery of islet
-produce glucagon -glucagon releasted in response to low blood glucose levels |
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beta cell death
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just know they die early
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UKPDS Study
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no matter what we do with type II it progressively gets worse
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regulation of beta cell mass
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pancreas trying for steady state
-beta cell signaling to maintain glucose homeostasis -increased hepatic glucose output |
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microvascular changes from diabetes
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-Retinopathy: lose vision QUICKLY, some don't know, 80-90% have it greater than 15 yrs, avg=10 yrs with diabetes and you don't know it
-Nephropathy: end stage renal disease, dialysis gives 10 yrs to live, more in minorities -Neuropathy: impaired sensation of feet and hands, slowed digestion in stomach, carpal tunnel, more than 60% of traumatic amputees |
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macrovascular complications with diabetes
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-80% of type II die of CVD->CHD
(angina, heart failure, attack) -cerebrovascular disease: stroke, TIA and 2-4 fold -peripheral vascular disease: gangrene, intermitten claudication, amputate |
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diabetic ketoacidosis
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worst case: decompensated system
-life threatening for type I and II -decreased insulin secretion -increased stress hormones -alpha cells are signaling bc beta arent fxning -release of free FAs, tissue breakdown to ketones -liver's not filtering, multisystem breakdown...Metabolic acidosis: CNS gives out, not shifting glucose to cells (brain)//COMA after passing out |
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dx for diabetic ketoacidosis
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intracellular glucose concentreation is low but if you finger pick it will be really high (capillary)
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cushing syndrome hallmark s/s
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buffalo hump on upper back
firm dark colored hirsutism |
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epidermis
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grows continuously by shedding superficial layers of stratum corneum
-2 types of cells: keratinocytes: keratin, skin hair and nails melanocytes |
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dermis
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1-4 mm thick with 3 layers
-collagen, elastin, ground substance |
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hypodermis/subq skin
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fat
capillary beds |
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dermal appendages
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nail
hair sebaceous glands |
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macule
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flat, circumscribed, color change
1 cm ex: moles, freckles, measles |
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papule
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elevated, firm, circumscribed
1 cm ex: wart |
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patch
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flat, irregular macule, non-palpable
> 1cm ex: vitiligo, port wine stain, birth mark |
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plaque
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elevated
firm rough > 1 cm psoriasis |
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wheal
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elevated, irregular shape, firm
ex: insect bites, allergic rxn hives etc |
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nodule
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elevated, firm, circumscribed, deeper than a papule into dermis
-1-2 cm ex: neoplasm, lipoma |
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tumor
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elevated, deeper into dermis
> 2 cm solid lesion ex: neoplasm, benign tumor, lipoma |
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vesicle
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elevated, circumscribed, superficial
-not in dermis, filled w/ serous fluid < 1cm ex: varicella, herpes zoster |
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bulla
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vesicle greater than 1 cm
blister |
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pustule
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elevated, superficial lesion, like a vesicle but filled with purulent fluid = acne
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cyst
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elevated, circumscribed, encapsulated, in dermis or subQ layer, filled with liquid or semisolid material
ex: cystic acne, sebaceous glands |
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telangiectasia
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fine, irregular, red lines produced by capillary dilitation
-esp in women over 40 yo ex: rosacea |
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scale
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heaped up keratinized cells, flaky, irregular pattern
ex: seborrheic dermatitis, dandruff |
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lichenification
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chronic dermatitis
rough, thickened epidermis -secondary to rubbing, itchy skin or irritation cell change |
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keloid
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elevated, irregular shape, enlarging scar, grows beyond bounds of wounds
-caused by excessive collagen formation IL-6 claw or star |
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scar
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thick or thin fibrous tissue
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excoriation
|
loss of epidermis, linear, crusted
ex: abrasions, scabies, scratches |
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fissure
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linear, crack or break from epidermis to dermis
-moist or dry ex: athletes foot, cracks side of mouth, candida yeast infection, diabetics |
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erosion
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loss of part of epidermis, depressed, moist, after a bulla or vesicle have erupted
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ulcer
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loss of epidermis and dermis
-decubitus |
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atrophy
|
thinning skin
aged skin striae, stretch mark |
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aging of skin
|
loss of elastin, collagen and fat density
-losing, shortening capillary loops -decreased melanocytes and langerhaans -genetic and envt |
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pressure ulcers
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result from any unrelieved pressure on the skin, causing underlying tissue damage
-pressure, shearing forces (sheets) -friction -moisture |
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stages of pressure ulcers
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non-blanchable erythema of intact skin (new shoes)
-partial thickness skin loss with epi and dermis (more serious) ex: pressure ulcer, cap bed gives way -full thickness skin loss involving loss of subQ tissue to bone |
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pruritus
|
most common s/s of primary skin disorders
-itch is carried by specific unmyelinated C-nerve fibers & triggered by a # of itch mediators -CNS can be modulated -pain stimuli at lower intensities can induce -chronic itching, deep infection |
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allergic contact dermatitis
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pruritus
erythema swell ex: poison ivy, oak |
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atopic dermatitis
|
type I hypersensitivity: activates mast cells, autoimmune
-causes red, weeping crusts and chronic inflammation |
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irritant contact
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non-immunologic inflammation
-chemical irritation from acids or prolonged exposure to an irritant |
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stasis dermatitis
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legs, venous stasis, edema, vascular trauma,
sequence: erythema pruritus brown scaling petechial ulcerations |
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psoriasis
|
silvery, shiny, rough patches than can turn to plaque
-many kinds, early and late -gutt -chronic, relapsing |
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lupus erythematosus
|
hyperimmune levels, biopsy for mast cells and leukocytes
-inflammatory, autoimmune disease with cutaneous manifestations -discoid: restricted to skin, photosensitivity (sun worsens) HALLMARK: butterfly pattern over nose and cheeks -systemic -chronic and no cure, suppresses immune system with steroids |
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folliculitis
|
strep infection at hair follicle
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furuncles
|
inflammatory at hair follicle
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carbuncles
|
collection of infected hair follicles
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cellulitis
|
infection of dermis and subQ
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erysipeias
|
acute superficial infection of upper dermis
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impetigo
|
superficial lesion caused by staph
-vesicle-like pattern -some pop and itch -treat with cream |
|
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herpes zoster
|
painful, follows nerves
-only ER situation because if it hits optic n. you'll go blind -virus attaches and is derived from nerve |
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herpes simplex
|
vesicular sac
follows nerve |
|
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warts
|
benign lesions caused by HPV
-Dx visually -condylomata acuminata: venereal warts |
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dermatophytes
|
superficial skin lesions
|
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mycoses
|
fungal disorders
|
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tinea
|
mycoses caused by dermatophytes
-capitis (scalp), pedis (foot)-look for fissures |
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candidiasis
|
normally on skin, GI, vagina
-C. albicans can change from commensal to pathogen |
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ways to tip scale that will increase yeast
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-antibiotics (dec vit K)
-moisture -warmth -pregnancy -DM -Cushings -age < 6 months -immunosuppression -neoplastic diseases |
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scleroderma
|
-tight facial skin
-fingers look like plastic,tapered and flexed -notice skin portion but not inside -can progress to internal organs (hypertrophy of heart, lungs kills with collagen deposits) -assoc w/ several antibodies -lesions exhibit -nails/fingertips can be lost from atrophy -mouth might not open completely -Lethal: 50% die within 5 years, lungs O2 dependent |
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cardinal sign of any respiratory problem
|
dyspnea
|
|
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s/s of pulmonary disease
|
dyspnea
orthopnea paroxysmal nocturnal dyspnea |
|
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dyspnea
|
subjective sensation of uncomfortable breathing
-air hunger, SOB, flaring nostrils -disturbances of ventilation/perfusion -fear and anxiety USING ACCESSORY M. TO BREATHE=INTERCOSTALS |
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orthopnea
|
dyspnea when a person is lying down
-increased SOB -SOB, preoccupation w/ breathing, worsening of dyspnea |
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paroxysmal nocturnal dyspnea
|
waking up at night w/ orthopnea
-LVH pts (hypertrophy) floppy left ventricle |
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kussmaul respirations
|
v. decreased RR assoc w/ severe met. acidosis like DKA
|
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|
kussmaul's sign
|
right sided, failure issue in heart
-pericardial enfusion at rt ventricle gets impinged -decreased JVP with deep breath and see it pop out, JVP (jug vein pressure) can't empty |
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cheyne-stokes respirations
|
caused by slowed blood flow to the brain stem
-alternating deep and shallow breaths -CO2 drives respiratory center...increased CO2 |
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s/s of pulmonary disease...hyper and hypoventilation
|
-hypoventilation: strangled, crushed airway
-hyperventilation: anxiety, breathe in paper back to conc. CO2ac |
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acute v chronic cough
|
acute: colds and flu
chronic: >1month, chest x-ray -ACE-I: angiotensin converting enzyme inhib, cuts off at ang-I, upregulates bradykinin, think drug therapy |
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hemoptysis
|
pink frothy sputum v dark (GI)
-hallmark of pulmonary edema |
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cyanosis
|
bluish discoloration of the skin and mucous membranes
-desaturated or decreased Hb of gums and lips -O2 deficit |
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pain assoc with pulmonary disease
|
pleura stretching during breathing
-specific, like a broken rib **manifestation of pulm. disease -activity, sharp and stabbing -pleural friction rub, squeaky just listen -pulmonary emboli can localize pain |
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clubbing
|
assoc with heart, lung disease, rounded bulbous fingers
-manifestation of chronic desaturation, not perfused with O2...distal to heart (fingers) 1-5 grading system -smokers can have it early -ex of lung disease: COPD, HD, kids get CF, pulm fibrosis) |
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abnormal sputum
|
color, odor, amt...smokers have more
-green=infection -bacterial exudate -bad smell is more tell tale |
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conditions caused by pulmonary disease/injury
|
-hypercapnea: increased CO2
-hypoxemia: decreased arterial O2, diff from hypoxia which is decreased perfusion to tissue -V/Q abnormalities |
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ventilation-perfusion abnormalities
|
V/Q= air reaches lungs/blood that reaches lungs
-shunting mismatch -alveolar capillary exchange isn't happening correctly |
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tissues that could cause V/Q on blood side
|
anemia
-a lot of diabetics -decreased volume of blood |
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acute respiratory failure
|
inadequate gas exchange that's hypoxemia when PaO2 is less than or equal to 50 or hypercapnea where pCO2 is > or equals 50 at a pH <= 7.25
-acute episodes of failure can happen w/ many respiratory diseases, ailments and ppl recover ex: mva, copd, lose a lung |
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pulmonary edema
|
-excess water in lung
-normally very little water in lung, lymp and cap beds keep it balanced via hydrostatic and oncotic P if they go up it takes O2 out -surfactant repels water around alveoli |
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what happens when hydrostatic P is greater than oncotic in lungs
|
fluid leaks from interstitium to alveoli
-lymph cant keep up -most common cause: CHD, esp LV failure*** |
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s/s of pulmonary edema
|
-dyspnea, orthopnea
-PINK FROTHY SPUTUM -hypoxemia and hypercapnea -crackles w/ auscultation -S3 gallop: ventricular dilitation, LV dysfxn, extra sound in lub dub, blood flow backwash - |
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respiratory center with pulmonary edema
|
chronic hypercapnea, gets used to high CO2 and low O2
-be careful when you put oxygen on bc of reset -high CO2 is normal for them and they won't breathe |
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s/s of COPD
|
-dyspnea, wheezing, sputum obstruction
-prob w/ forced expiration -alveoli are hyperexpanded because they don't exhale, back pressure, bronchial tubes can't exhale as well=dec elasticity **-smokers miss cilia |
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hallmark of COPD
|
barrel chest: almost hunched over so they can expand thorax maximally
-lat view, measure distance from mediastinum to spine -position brings an adaption |
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asthma
|
IGE pathway, allergic experience
-prominent inflamm process -chronic presence of mast cells and others promote a fibrotic state which evolves to permanent changes in lung basement membranes: abnormal lung fxn -familial/genetic w/ 20 genes ID'd |
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asthma risks
|
1st and 2nd hand smoke
urban areas allergens recurrent viral infection **bronchial airways are hyperreactive |
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|
treatment for asthma
|
measure with peak flow meter
-long acting bronchodilators, corticosteroid, leukotriene inhibitors -fast acting inhaler for emergences |
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|
status asthmaticus
|
severe bronchospasm
work of breathing is 5-10x more life threatening...intibate and roids |
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chronic bronchitis
|
-hypersecretion of mucus, more color changes and sputum smells
-chronic productive cough that lasts for at least 3 mos/yr for 2 consecutive years -inspired irritants makes more mucus and size and # of mucus gland sincreases -smokers, workers near pollutants -recurrent resp infection is common so get immunizations |
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emphysema
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abnormal permanent enlargement of the gas-exchange airways accompanied by destruction of alveolar walls w/o obvious fibrosis destruction of air sacs is permanent
-tobacco, toxic chem exposure -lose elastic recoil |
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s/s of emphysema
|
dyspnea
DOE LITTLE sputum decreased cough tachypnea barrel chest |
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conditions caused by pulmonary disease or injury
|
aspiration
atelectasis bronchiectasis |
|
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aspiration
|
passage of fluid and solid particles into lungs
-GI fluid into lungs like e.coli is life threatening |
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|
atelectasis
|
compression, tumor, fluid
absorption: lung increased O2, face mask, bagging, kids, overinflate -air in pleural space becomes dead space, could make chronic and COPD Dx **interference w/ MECHANISM |
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|
bronchiectasis
|
persistent abnormal dilation of the bronchi after an infection or virus
-cylindrical, saccular, varicose (smooth muscles wrapped around bronchi to help exhale, twist and get too tight) -common in kids, RSV is most common presentation -chronic bronchitis in adults can lead to this |
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hallmark of bronchiectasis
|
barking cough
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pneumothorax
|
open, losing 1/2 lung space
-pressure shifts, like gun shot destroys air P -usually affects 1 lung - |
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|
hallmark of pneumothroax
|
mediastinal shift to unaffected area
|
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tension pneumothorax
|
tumor (invasive), surgery
-pressing and lungs give up to higher pressure |
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|
spontaneous pneumothorax
|
infrequent
collapses and you dont know why |
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secondary pneumothorax
|
MVA
resp distress syndrome body rxn to accident -not pressure related -in response to a disease or accident |
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|
pleural effusion
|
transudative and exudative
-lung can't expand, not collapsed -pleurisy: chronic inflammation -hemothorax |
|
|
tx of pleural effusion
|
antibiotics IV
|
|
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empyema
|
infected pleural effusion
pus-sac |
|
|
abscess formation
|
-abscess
-consolidation: evolution of fibrosis, longer time, hardening -cavitation: lung eaten through to chest wall, breast cancer too, no way back usually=OUTWARD EXPRESSION |
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|
pulmonary fibrosis
|
excessive amt of fibrous or CT in the lung
-no reason |
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chest wall restriction
|
compromised, not perfusing
-deformation (organs not where they should be), immobilization and/or obesity |
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|
flail chest
|
gunshot
open pneumothorax Hallmark: mediastinal shift to unaffected area |
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|
acute respiratory distress syndrome
|
fulminant form of resp failure characterized by acute lung inflamm and diffuse alveolar cap injury
-injury to pulm cap endothelium -atelectasis -surfactant inactivation |
|
|
manifestations of acute respiratory distress syndrome
|
rapid
shallow breath |
|
|
post-op resp failure
|
atelectasis: P on lung
pneumonia pulmonary edema pulmonary emboli |
|
|
prevention of post op respiratory failure
|
frequent turning
deep breathing early ambulation air humidification incentive spirometry |
|
|
community acquired pneumonia
|
difficult to rid, adapted to antibiotic
-mycoplasm in college and HS streptococcus pneumoniae |
|
|
pneumococcal pneumonia
|
can see in aspiration, bacteria instant colonization
-steroids to suppress strep -produce sputum--congestion -fibrin in pleural space, phagocytosis |
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|
types of pneumonia
|
community acquired
viral nosocomial pneumococcal |
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|
pulmonary embolism
|
occlusion of a portion of the pulm-vasc bed by a thrombus, embolus, tissue fragment, lipid plaque, air bubble from IV
-commonly from deep veins in thigh DVT BC pills |
|
|
s/s of pulmonary embolism
|
chest pain at exact spot
v/q on perfusion side dyspnea lower PaO2 pulmonary infarction systemic shock |
|
|
tuberculosis
|
mycobacterium tuberculosis
-acid fast bacillus airborne transmission tubercle formed (tumor) caseous necrosis -+ PPD tuberculin skin test |
|
|
primary pulmonary hypertension
|
idiopathic
|
|
|
secondary pulmonary hypertension
|
diseases of resp system and hypoxema are more common causes
-didnt treat HTN obese (hypoventilated) chronic hypoxia don't know why we constrict pulmonary artery |
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|
hypersensitivity reactions
|
exaggerated responses to an anitgen
can be immediate or develop within hours |
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|
allergy
|
exaggerated response to environmental antigens
dust, mold, pollen |
|
|
autoimmune
|
exaggerated response to your own antigens
-host misdirecting response at itself |
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|
alloimmune
|
exaggerated response to other person antigens
-when you have a transfusion and you react to the blood you are receiving |
|
|
mechanisms of hypersensitivity rxns are classified as
|
-type I: IgE mediated rxns
-type II: tissue specific rxns -type III: cell mediated rxns |
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|
anaphylaxis
|
a response from one the hypersensitivity rxns (type I-III)
-most rapid of all rxns, can be life threatening -usually an explosive rxn, type I IgE pathway |
|
|
tx for anaphylaxis
|
epinephrine, works on several levels of the rxn but does essentially relax constricted airways, BV's
|
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|
scratch testing
|
many antigens are impregnated small gauge needles are put onto the back all at once, usually 60 on a board are put onto the back
-see which react and they're + allergens |
|
|
tx for allergies
|
-desensitization: admin very small doses of the allergen over time to give repeated exposure (mildy effective)
-mast cell stabilizers -antihistamines |
|
|
systemic lupus erythematous
-who is affected more -links -whats happening |
-chronic multisystem, inflammatory disease
-most common, complex and serious autoimmune disorders -auto-antibodies are working against nucleic acids(DNA, RNA etc) -produces tissue damage: kidneys esp glomerulus -occurs mostly in women esp 20-40 yo (10:1) -blacks affected more than whites -prob a genetic link |
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|
s/s of systemic lupus erythematous
|
arthralgias
arthritis vasculitis rash renal disease hematologic abnormalities CV disease |
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|
alloimmune graft rejections
|
transplant of organs commonly is complicated by an immune response against antigens, primarily HLA (human leukocyte antigen), part of the histocompatibility complex
-HLA typing is done prior to transplant to check donor/recipient matching and enhances the probabilty of acceptance -rejection can be hyperacute (still on the OR), acute (days-mos), or chronic (mos-yrs) |
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|
transfusion reactions (alloimmune)
-blood types and their antibodies |
RBC's express several surface antigens known as blood group antigens which are targets for alloimmune rxns
-A, B, AB,O -A have antibodies to B -B have antibodies to A -AB is universal recipient -O is universal donor -transfusions=antigens so antibodies form |
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|
Rh factor...% of ppl
|
type of protein on the surface of RBC's
-more than 85% of ppl are + |
|
|
what happens if someone is Rh negative and pregnant?
|
-you can develop antibodies to an Rh+ baby
-if your blood mixes with fetal your body could respond like an allergic rxn -body can make antibodies to attack Rh antigens in baby's blood by crossing placenta, which means you are sensitized -they breakdown fetal RBC's and cause anemia (hemolytic disease/anemia) |
|
|
complications and Tx when Rh factors dont match up for mom and baby
|
serious illness
brain damage even death in fetus or newborn -prevent with meds called immunoglobulin (RhIg) |
|
|
Sensitization can occur any time a fetus's blood mixes with the mother's. it Can occur in an Rh negative woman if she has had...
|
-miscarriage
-induced abortion or menstrual extraction -ectopic pregnancy -chorionic villus sampling -blood transfusion |
|
|
how can problems with Rh factor and pregnant woman be prevented
|
blood test can provide your type and Rh factor
-antibody screen to show if an Rh negative woman has antibodies to Rh positive blood -injection or Rh immunoglobulin: blood product that can prevent sensitization of an Rh-negative mother |
|
|
when is RhIg used
|
-woman w/ Rh neg hasn't been sensitized, get at 28th week to prevent sensitization for rest of preg
-baby born with Rh pos, mother should take dose to prevent antibody formation to Rh pos cells she could get from baby before and during delivery -only good for the preg which its given -Rh neg women after miscarry, ectopic preg or induced abortion to prevent any chance of developing antibodies for Rh pos future baby |
|
|
other reasons RhIg is given other than pregnancy
|
-amniocentesis: fetal Rh pos could mix with neg and mom would produce antibodies
-Rh neg mom after birth if she wants tubes tied and cut b/c she might try to later have sterilization reversed, might fail to prevent preg, blood transfusion need |
|
|
what happens if antibodies develop with preg mom
|
-RhIg doesn't help once mom develops antibodies..if the mom is sensitized they check fetus for condition
-baby may be delivered on time, blood transfusion for the baby to replace diseased blood cells -severe: baby delivered early or give transfusions while in uterus |
|
|
primary impaired fxn of immunity/inflamm response
|
genetic defects that disrupt leukocyte development
-congenital |
|
|
secondary impaired fxn of immunity/inflammatory response
|
acquired
-due to disease or pathological alteration |
|
|
ex of deficiencies in immunity...primary secondary etc
|
SCID: severe combined immune deficiency, total lack of T-cell fxn and severe lack of B-cell fxn
-AIDS -missing antibody production is treated by replacement of immunoglobulins |
|
|
#1 world wide cause of death
|
infection:
plague cholera malaria TB leprosy schistosomiasis |
|
|
small pox
polio whooping couch |
small pox eradicated from glvoe
-polio in western hemi by vaccination -whoop cough back due to non-complance with vaccines |
|
|
new infectious diseases
|
west nile virus
H1N1 severe resp syndrome (SARS) lymes hantavirus HIV drug resistant TB |
|
|
stages of infection
|
1. colonization
2. invasion 3. multiplication 4. spread |
|
|
what influences pathogens
|
-mechanism of action, direct damages to cell wall
-infectivity: ability for pathogen to invade -pathogenicity: ability to produce disease -virulence: potency of pathogen -immunogenicity: how it induces an immune response -toxigenicity: exo and endotoxins -portal of entry: inhale,ingest,bite |
|
|
symbiois
|
benefits only human
no harm to organism ex: vaccines |
|
|
mutualism
|
benefits both organisms
-biologics |
|
|
commensalism
|
benefits only organism but no harm to human
-pathologic |
|
|
pathogenicity
|
benefits organ
harmful to human ex; malignancy |
|
|
bacteremia/septicemia
|
presence of bacteria in the blood and is caused by a failure of body's defense mechanisms
-usual cause is gram neg bacteria and some gram pos or fungi |
|
|
consequences of bacteremia/septicemia what happens to body and how to dx
|
endotoxins are produced which trigger cytokines = vasodilation of BV's, decreased BP, O2, and temp = SHOCK...cardiogenic
-blood cultures are dx -usually fatal |
|
|
how do viruses cause significant illness
|
enter host cell and use metabolic processes to proliferate, can change to cancer cell and people dont know how
|
|
|
mycoses
|
diseases caused by fungi
-fungi grow as parasites on or near the skin or mucous membranes and produce mild and superficial disease of the hair, nails, scalp |
|
|
vaccines
|
prevent disease by inducing a primary and secondary immune response under conditions that will not result in disease
-exist to prevent certain viral and bacterial infections -viral vaccines usually contain attenuated live viruses but most bacterial are killed organisms or bacterial antigens |
|
|
why do you get boosters for vaccines
|
to stim large number of memory cells in the immune system to produce more antibodies-secondary response
|
|
|
antibiotics...how resistance can develop etc
|
through genetic mutations that inactivate the drug int eh presence of a bacteria
-overuse can lead to disruption of normal flora allowing for selective overgrowth...often in gut and other bacterias that normally would be killed can take over...C. difficile =overwhelming diarrhea |
|
|
general adaptation syndrome with stress...non-specific physiologic response
|
stage 1-alarm
stage 2- resistance or adaption stage 3- exhaustion |
|
|
stress response is initiated by
|
CNS system
endocrine system |
|
|
limbic area of brain and response to stress etc
|
stims neural paths responsible for receiving sensory info, and eliciting a central response directly by stimulation LC to release norEpi and Epi...increase CO, BP, dilate bronchus
--> stims hypothalamus to secrete ACTH which stims adrenal coretx to secrete cortisol |
|
|
what does cortisol release due
|
mobilizes energy (glucose) and promotes formation of gluc, AA's, lipids and FA's and delivers them to the bloodstream.
-This stims insulin production which acts to help use gluc in cells but it stores FFAs as fat in the body as a stress response |
