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patho final Flashcards

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1
Q

atrophy

A

decreased workload

decreased cell size

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2
Q

hyperplasia

A

increased number of cells

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3
Q

hypertrophy

A

increased workload

increased cell size

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4
Q

benign

A
  • usually harmless
  • almost always encapsulated
  • prevents the release of cells, restricting the spread
  • problems are related to compression
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5
Q

malignant

A
  • rapid, uncontrolled and disorganized growth
  • metastasis
  • starve normal cells
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6
Q

hypersensitivty reactions

A
  • inappropriate response to antigen
  • occurs immediately or within minutes to hours
  • classified by pathogenesis
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7
Q

type 1 hypersensitivty

A

immediate reaction
- had to have been previously exposed (sensitization)

1st exposure: IgE: antibodies are made and attach to mast cells through the body

2nd exposure: antigen causes IgE to trigger T cells and histamine

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8
Q

type 11 hypersensitivity

A

cytotoxic and cytolytic reaction
- igG and igM antibodies bind with antigen on cell surface

  • cell destruction occurs
  • resulting in: Lysis, phagocytosis
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9
Q

type 3 hypersensitivity

A
  • immune complex reactions: antigen-antibody complexes
  • ineffectively removed by phagocytosis
  • autoimmune diseases
  • sites: kidneys, skin, joints, blood vessels. and lungs
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10
Q

type 4 hypersensitivity

A
  • cell-mediated or delayed hypersensitivity reactions. mediated by t cells as opposed to antibodies
  • occurs in two phases
  • sensitization phase
  • effector phase
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11
Q

neutropenia

A
  • decrease neutrophil- leads to more infections
  • normal: 2,000-7,500 cells/ml
  • causes: increase use infection, decrease production
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12
Q

thrombocytopenia

A

low platelets

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13
Q

anemia

A
  • decrease in rbc
  • decrease in hemoglobin content
  • abnormal Hgb

results from:

  • impaired production
  • increased destructing
  • blood loss

leading to
- decreased oxygen-carrying capacity

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14
Q

anemia cm

A
  • weakness
  • fatigue
  • pallor
  • syncope
  • dyspenea
  • tachycardia
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15
Q

iron deficiency anemia

A
  • low iron
  • decrease hgb production
  • decrease absorption (upper gi tract)
  • increase bleeding (menstruation)

prevalence

  • women of childbearing age
  • children under 2
  • elderly

diagnosis

  • cbc
  • ferritin
  • iron
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16
Q

pernicious anemia

A
  • b12 deficency or megaloblastic anemia
  • decrease cyancobalmin b12
  • lack on intristic factor
  • acquired: portion of stomach/intestines

autoimmune

  • destruction of pareital cells
  • results in immature rbcs

diagnosis

  • cbc
  • vitamin b12
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17
Q

aplastic anemia

A
  • destruction of bone marrow
  • resulting from variety of factors

autoimmune conditions

  • medications
  • viruses
  • toxins
  • genetic abnormalities
  • pancytopenia: low rbc, wbcs, plts
  • increase clinical manifestations

diagnosis

  • cbc
  • bone marrow biopsy
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18
Q

hemolytic anemia

A
  • destruction (hemolysis of rbc

multiple types

  • sickle anemia
  • thalassemia- rare
  • erthryoblastosis- children
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19
Q

sickle cell anemia

A
  • inherited autosomal recessive
  • hgb becomes sensitive to changes in 02
    • changes from disk shape to crescent shape
  • not able to flow through vessels leading to clumping
  • only live for 20 days instead of 120 days
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20
Q

signs and symptoms of sickle cell anemia

A
  • severe pain and swelling
  • abdominal pain
  • tachypnea
  • dilute urine and blood in the urine
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21
Q

sickle cell diagnosis

A
  • sickledex test

- hemoglobin electrophoresis

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22
Q

neutropenia diagnosis and treatment

A
  • complete blood count
  • bone marrow biopsy

treatment
- causative in nature: need to know underlying cause treatment

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23
Q

neutropenia

A
  • decrease neutrophil- leads to more infections
  • normal: 2,000-7,500 cells/ml
  • causes: increase use infection, decrease production
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24
Q

clinical manifestations of neutropenia

A

fever
chills
fatigue

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25
regurgitation
- valve does not close completely | - blood flow backs up
26
stenosis
- narrowed, valve does not open completely - forward blood flow hindered - decreases cardiac output
27
right- sided heart failure
- left-sided heart failure major cause must continually pump blood against increased fluid in the pulmonary artery and lungs - cor pulmonale: right ventricle hypertrophies and fails due to increased pulmonary pressures - a backward buildup of blood systematic blood vessels - peripheral edema results - backs into body= edema, jugular vein distension - body can attain a liter of fluid before showing signs: weigh pt.
28
left- sided heart failure
- afterload: force generated by left ventricle to eject blood to the aorta through aortic valve - peripheral vascular resistance: pressure within aorta/arteries - pvr influences afterload - hypertension major cause - blood backs up from left ventricle into lungs into pulmonary circulation= flooded capillaries - avelora edema
29
atherosclerosis
thickening/ hardening of arterial walls from plaque formation - may begin in childhood
30
coronary artery disease (CAD)
obstruction of blood flow through coronary arteries typically caused by atherosclerosis can cause: - angina - myocardial infarction - sudden death
31
myocardial infarction
death of heart muscle types - non-st segment elevation myocardial infarction (NSTEMI) - st segment elevation myocardial infarction (STEMI) etiology - atherosclerosis: narrowing of coronary arteries - thrombus: embolism - vasospasm: constriction
32
hypertension
persistently high blood pressure - systolic BP > 130 mmhg - diastolic bp > 80 mmhg - average of two or more readings on different dates: two weeks apart
33
patho of mi
- coronary artery blockage | - decreased cardiac blood supply
34
signs and symptoms of mi
- crushing viselike pain arm, shoulder, neck, jaw, back - shortness of breath - restlessness - dizziness, fainting - nauesea - sweating
35
atypical signs of MI
- abscne of classic pain - dyspena - fatigue - anxiety - impending doom - chest cramps - abdominal pain - indigestion - restlessness - falling
36
prehospital MI
"time is muscle" - asprin - call 911 of 5 min of chest pain - do not drive
37
hospital MI
Morphine Oxygen Nitroglycerin Aspirin
38
CAD prevention
- non-modifiable risk factors: age and family modify risk factors - tabacco use - obesity - inactivity - stress - dm - hld - htn
39
patho of atherosclerosis
- injury to artery--> inflammation--> accumulation of lipids, platelets and clotting factors - scar tissue replaces normal endothelial lining - plaque leads to narrowing (stenosis)
40
non-modifiable risk factors of ac
- age: 50+ - gender: male - ethnicity: African Americans - genetics
41
modifiable risk factors of ca
``` diabetes hypertension smoking obesity sedentary lifestyle increased serum homocysteine increased serum iron levels infection depression hyperlipidemia excessive alcohol intake stress ```
42
hypertension
persistently high blood pressure - systolic BP > 130 mmhg - diastolic bp > 80 mmhg - average of two or more readings on different dates: two weeks apart
43
etiology of hypertension
unkown two types: - primary- essential hypertension which is a chronic elevation of bp from an unknown cause ``` - secondary known cause - acute stress - excessive alcohol intake - sickle cell disease - renal disorders - endocrine disorders - neurologic ```
44
risk of hypertension
non modifiable - age - gender - ethnicity - family history modifiable - alcohol - cigarette smoking - diabetes - obesity - stress - elevated serum lipids - excess dietary sodim - decreased kidney function
45
signs/ symptoms of HTN
silent killer rare: - headache - dizziness - blurred vision - angina - fatigue - dyspena
46
hypertensive urgency
- sever bp elevation without target organ dysfunction progression - relatively asymptomatic - oral medication
47
hypertensive emergency
- sbp> 180 mm hg systolic - dbp > 120 mm hg systolic - risk for progression for target organ dysfunction - immediate gradual reduction of bp to protect target organs
48
what is pneumonia
- an infection that inflamed the lungs and impairs gas exchange - air sacs fill with fluid causing cough and difficulty breathing
49
patho of pneumonia
development occurs when a pathogen reaches the alveoli and host defesnes are overwhelmed by microorganisms or by the inoculum size
50
pneumonia diagnosis symtoms
- ineffective airway clearance - impaired gas exchange - ineffective breathing pattern - risk for infection - acute pain
51
pneumonia etiology
1. infectious agents A: bacteria and viruses that are usually inhaled - infection gets into lungs causing inflammation - steptococcus pneumoniaw is responsible for most cases of pneumonia B: fungi ``` 2. injurious agents A: aspiration - gastric contents B: endotracheal intubation C: smoke - inhalation of smoke or chemicals ```
52
clinical manifestations pneumonia
- hypoxemia - cough - fever - rapid and shallow breathing - loss of appetite - abnormal lung sounds - fatigue - chest pain - dehydration - clammy skin - difficult or labored breathing
53
pt. teaching pneumonia
- what exactly pneumonia is - different stages of pnemonia - when/how to take medications - what the medications are used for
54
pneumonia prevention
- many different pneumonia vaccines - flu vaccines - quit smoking - wash hands often - maintain healthy lifestyles
55
medications/treatment pneumonia
- macrolide medications - oral antibiotics - antiviral medications - over the counter meds - hospitalization - oxygen therapy
56
asthma clinical manifestations
- Shortness of breath. - Chest tightness or pain. - Wheezing when exhaling, which is also a common sign of asthma in kids. - Trouble sleeping caused by shortness of breath, coughing or wheezing. - Coughing or wheezing attacks that are worsened by a respiratory virus, such as a cold or the flu. - being too breathless to eat, speak or sleep. - breathing faster. - a fast heartbeat. - drowsiness, confusion, exhaustion or dizziness. - blue lips or fingers. - fainting.
57
patho of asthma
- inflammed airways react to environmental triggers such as smoke, dust, pollen - airway epithelial cells, which are the first line of defense against inhaled pathogens are partiles, initiate airway inflammation and produce muscous - leads to coughing and breathign dificulties - airway narrows - result of immune response in the bronchial airways - in response bronchi contract into spasm
58
genetic predisposition of asthma
- more than 100 genes associated with allergic asthma - offspirng of asthmatic parents - ORMDL3 gene associated with childhood onset - HLA-DQ gene was related to later onset asthma
59
treatment of asthma
- symptoms controlled - inhaled and systemic corticosteroids: supress airway inflammation - bronchiodilators - leukitriene - mast cell stabilizer - anticholinergics
60
diagnosis of asthma
- lung function test | - chest or sinus x ray
61
pt teaching of asthma
- properly teach pt. how to use inhaler - take asthma medication directly as your provider tells u - be sure to always have a quick- relief inhaler - watch for early changes of symptoms getting worse by using a peak flow meter - use dust proof covers - dont smoke - try to keep window closed during pollen seasons
62
COPD risk factors
- exposure to tobacco smoke - exposure to dust and chemicals - exposure to fumes from burning fuel - people with ashma - genetics
63
COPD treatment
- bronchodilators | - steroids
64
diagonsis of COPD
- pulmonary function test - spirometry - chest x-rays and ct scans
65
patho of COPD
- combined process of narrowing airways- limitd airflow and causes loss and destruction of aveloi, bronchioles, and surrounding capillary vessels - lung capacity further decreases - reduced airflow - dyspnea - hypercapina
66
etiology of COPD
smoking and people exposed to fumes, like carbon monoxide or chemicals - alpha-1 antitrypsin genetic link to copd two causes: - emphysema - chronic bronchitis
67
prevention of copd
- no prevention - getting flu vac - quit smoking
68
clinical manifestations of copd
- shortness of breath - wheezing - chest tightness - lack of energy - weight loss - chronic cough - edema - anorexia
69
pleural effusion
accumulation of excess fluid in the plerual space or pleura (membranous linning of the lungs and chest cavity)
70
normal fluid in lungs
- 10-20ml of fluid - lubricates lungs - decreases friction
71
patho of pleural effusion
- excessive fluid in small space - compresses lungs - limits expansion during inhalation - can affect one or both lungs - various types of fluid can accumulate in a variety of locations
72
what can accumulate in pleural effusion
- exudative: protein- rich fluid - transudative: watery - hemothorax: blood - pneumothorax: air - empyema: pus
73
etiology pleural effusion
- heart failure - pulmonary embolism - cirrhosis - pneuminia - kidney disease - cancer - bleeding
74
diagnosis pleural effusion
xray ct scan ultrasound
75
clinical mafiestations pleural effusion
- dyspnea - pleuritic chest pain - tachypnea - tracheal deviation - pleural friction rub - tachycardia - dminished/absent lung sounds
76
pleural effusion treatments
- depends on s/s - some resolve w/o tx - correct underlying cause - remove excess fluid: thoracentesis, chest tube - antibiotics
77
atelectasis
incomplete alveolar expansion or collapse of the alveoli
78
normal for alveolo
- alveoli expand - has exchange - o2 is brought in during inhalation - co2 is expelled during exhalation
79
patho of atelectasis
- walls of alveoli stick together | - prevents adequate gas exchange
80
etiology atelectasis
- surfactanr deficiency- prevents aveloi from sticking together - bronchus obstruction - compression of lung tissue - lung fibrosis
81
risk factors atelectasis
- surgery | - inmmobility
82
clinical manifestations atelectasis
- tachypnea - decrease breath sounds - dyspnea - anxiety - restlessness - tachycardia - asymmestrical chest expansion
83
prevention of atelectasis
- increase mobility - breathing exercises - cough and deep breaths - inventive spirometry - pain management
84
treatment of atelectasis
- antibiotics - thoracentesis - incentive spirometry - bronchodilator
85
hypervolemia
excess fluid in the intravascular space
86
water intoxication
excess fluid in the intracellular space
87
causes for excess fluid
excessive sodium or water intake - high sodium diet - psychogenic polydipsia - hypertonic fluid administration - free water - enteral feedings inadequate sodium or water elimination - system/ organ failure (renal, liver, heart) - endocrine disorders (hyperaldosteronism, crushing syndrome, syndrome of inappropriate antidiuretic hormone
88
clinical manifestations for excess fluid
- edema( peripheral, perorbital, cerebral) - dyspnea - bounding pulse - tachycardia - jvd - htn - polyuria - weight gain - crackles
89
diagnosis for excess fluid
- H&P - daily weights - I&O - labtest (CBC, chemistry) - urinary analysis
90
treatment for excess fluid
- compression socks - diuretics - restricting NA - fluid restriction - hypertonic solutions
91
Fluid imbalance- deficit
- dehydration - hypovolemia or fluid volume deficit - decreased fluid in the intracellular space - can occur independently without electrolyte defects
92
fluid imbalance deficit reasoning
inadequate fluid intake - poor oral intake - inadequate iv fluid replacement excessive fluid or sodium losses - gastrointestinal losses - excessive diaphoresis - prolonged hyperventilation - hemorrhage - nephrosis - diabetes mellitus - diabetes insipidus - burns - open wounds - ascites - effusions - excessive use of diuretics - osmotic diuresis
93
fluid imbalance deficit clinical manifestations
- thirst - altered LOC - hypotension - tachycardia - weak/thready pulse - dry mucous membranes - tenting skin turgor - oliguria - weight loss - sunken fontanelles
94
fluid imbalance deficit diagnosis
- h&p - daily weights - I&Os - lab test (cbc & chemistry) - U/A
95
deficit treatment
- identifying/ managing underlying cause | - replacement fluids
96
hyponatremia
sodium < 135 mEq/l | - serium osmolarity decreases
97
hyponatremia causes
deficient sodium - too much: diuretics, Gi loss (V/d), diaphoresis - not enough in: Na restricting excessive water - too much in: hypotonic solutions, oral hydration - not enough out: renal failure, heart failure, SIADH
98
hyponatremia clinical maifestations
- GI upset - lethargy - confusion - decrease deep tendon reflexes - muscle weakness - seizures - coma
99
hyponatremia diagnosis
- serum Na level | - urinalysis
100
hyponatremia treatment
- fluid restriction | - increase dietary Na
101
hyperkalemia
potassium > 5 mEq/l
102
hyperkalemia causes
- deficient excretion: renal/ liver failure, medications - excessive intake: oral K supplements, rapid IV administration - lot of older adults defficent - check inf they are on a diuretic
103
hyperkalemia clinical manifestations
- paraesthesia - muscle weakness - respiratory depression - EKG CHANGES ( dysrthmias) need to shock them - cardiac arrest - abdominal cramping
104
hyperkalemia diagnosis
- serum k levels | - EKG
105
hyperkalemia treatment
- decrease intake - hold supplements - medications: diruects, kayexalate, insulin - telemetry monitoring (continuous way to monitor EKG)
106
Incontinence
loss of urinary control | - affects 25-35% of population
107
types of incontinecne
children - enuresis - nocturnal enuresis adults - stress - urge - reflex - overflow - functional - treatment
108
incontinence children enuresis
involuntary urination by a child after 4-5 years of age
109
incontinence children nocturnal enuresis
- bed wetting types - primary: child never developed normal bladder control @ night. might bc bladder too small - secondary: normal urinary control. physiological causes changes it causes: - psychological - structural - underlying condition
110
incontinence adulthood stress
- combined process of weakening of bladder sphincter and intra-abdominal pressure contributing factors: - pregnancy - child birth - menopause - prostate removal and obesity
111
incontinence adulthood urge
- sudden, intense urge to urinate and involuntary loss of urine - overacting bladder - few second warning causes - parkinson - alzheimer disease - stroke - injury to nervous system - frequent uti
112
incontinence adulthood reflex
trauma or damage to nervous system - detrusor hyperreflexiaxia - increased detrusor muscle contractility - urine is released bladder cant relax and fill
113
incontinence adulthood overflow
- inabilty to empty bladde ror retention - chronic distention - "nursing/teaching bladder" causes: - bladder damage - urethral blockage - nerve damage - prostate conditons
114
incontinence adulthood functional
- physical or mental impairment that prevents toileting in time
115
incontinence transient
- resulting from underlying cause - temporary causes - delirium - infection - use of diuretics and sedatives - high urine output - alcohol and caffeine consumption
116
risk factors for incontinence
- female gender- pelvic floor muscle and vaginal wall weakening - advancing age- both muscle weaken and urine storage - obesity - smoking
117
complications innocence
- impaired skin integrity - recurrent utis - impaired body image/ sexual disfunction - interruption of usual activities
118
benign prostatic hyperplasia (BPH)
nonmalignant enlargement of the prostate gland
119
benign prostatic hyperplasia (BPH) etiology
- unknown --> decreased testosterone | - common over age 50
120
benign prostatic hyperplasia (BPH) patho
- abnormal proliferation --> enlargement of prostate - compression of urethra --> obstruction of urine flow - urine collects in bladder causing uti and thickening of bladder
121
benign prostatic hyperplasia (BPH) risk factors | o-dice
``` obesity cardiovascular disease DM2 inactivity ED ```
122
acute kidney injury
sudden loss of renal function - days to weeks - generally reversible
123
acute kidney injury etiology
inadequate renal perfusion - prerenal (before kidney)- decrease bp, HF - intrarenal (within kidney)- inflammation of glomerulus/ compression on internal structures - postrenal (after kidney)- urethral/ bladder obstruction- interfere with the ability to secrete urine
124
acute kidney injury patho
- abrupt onset | - 4 phase process
125
acute kidney injury lab values
creatinine increase - decreased urinary excretion - waste product produced by muscle BUN increase - decreased urinary excretion
126
acute kidney injury phases
- prodromal - oliguric - diuretic - recovery
127
acute kidney injury phases: prodromal
- damage occurs | - pt. asyomptomatic
128
acute kidney injury phases: oliguric
- nephrons are damaged - decreased glomerular filtration - decreased urine output - less than 400 ml/day
129
acute kidney injury phases: diuretic
- renal function begins to improve - tubular damage continues to impair ability to concentrate urine appropriately - leads to diuresis- excess urine output (depletes fluids and electrolytes) - up to 5l
130
acute kidney injury phases: recovery
- can take 3-12 months | - glomerular filtration returns to normal
131
chronic kidney disease
gradual, irreversible loss of renal function - nephrons become injured - replacement by scar tissue - affects 30 million adults
132
chronic kidney disease etiology
- DM- diabetes #1 cause - HTN- affects glomelura - urinary obstruction- increase pressure on kidneys - renal artery stenosis- not good blood flow - nephrotoxic medications- kidney toxic (NSAIDS) - sickle cell disease - SLE- sickle cell attacks cells in nephron - smoking- harden Bu- small Bu in kidneys - aging- less effective
133
chronic kidney disease patho
damaged nephrons --> impaired kidney function - decrease regulation and ability to eliminate waste products and drug exretion - increase bp
134
chronic kidney disease stage 1
kidney damage present by GFR > 90
135
chronic kidney disease stage 2
kidney damage worsens as the GFR falls (60-89)
136
chronic kidney disease stage 3
kidney function is signficantly impaired as GFR is between 30 and 59
137
chronic kidney disease stage 4
kidney function is barley present with GFR dropping between 15 and 29
138
chronic kidney disease stage 5
kidney failure as the GFR drops to less than 15
139
gastroesophageal reflux disease
chyme or bile periodically backs up from the stomach into the esophagus
140
patho gastroesophageal reflux
- gastic secretions reflux into esophagus - esophaguses damaged - lower esophageal spincter does not close tightly
141
gastroesophageal reflux risk factors
- foods (chocolate, citrus fruit, spicy or fatty foods) - beverages (caffeine, carbonated beverages, alcohol) - medical conditions (hiatal hernia, obesity, pregnancy)
142
gastroesophageal reflux clinical manifestations
- heartburn or epigastric pain - dysphagia - sensation of a lump in throat
143
cholecystitis
inflammation of galbladder
144
cholelithiasis
stones
145
choledocholithiasis
stones in CBD- common bile duct | first two happen independtly
146
gallbladder disorders risk factors
- age - obesity - diet (increase fat, increase cholesterol, decrease fiber) - pregnancy: after delivery= change in nutritional status - chronic diseases (of hypatbillary system)
147
gallbladder disorders clinical manifestations
- biliary colic- specific pain in RUQ radiates to shoulders and back after fatty meal - RUQ pain - n/v when stone lodged: - jaundice - chronic disease
148
hepatitis
inflammation of liver etiology - viral or bacterial infections - drugs - alcohol - hepatotoxic drugs - metabolic/ vascular disorders
149
hepatitis types
- HAV- most common transmitted tru frcal oral route - HBC- transited thru blood, sexually transmited fluids: blood, stool, urine, saliva - HCV- transmitted thru blood, Iv drug use (not really seen anymore) use to associated with blood tranfusions - HDV- extremely rare - HEV- extremely rare
150
hepatitis prevention
- hand hygiene | - vaccines: hav, hbc
151
cirrhosis
progressive, irreversible replacement of healthy tissue with scar tissue - 12th leading cause of death in US
152
cirrhosis etiology
- chronic alcohol use- most common - hepatotoxins drugs - hepatitis- left untreated - gallbladder obstruction- prolonged - heart failure
153
cirrhosis patho
- inflammation of liver cells - infiltration with fat and wbc - fibrotic scar tissue replacements liver tissue - abnormal regeneration - impaired liver blood flow and function
154
cirrhosis complication
- clotting defects - encephalopathy: elevation of ammonia portal hypertension - varices: enlarged vessels- risk for rapture: coughing/ vomitting can cause repture - ascites: fluid accumulation in addomen: fluid not being held in vascular system
155
appendicitis
inflammation of appendix patho - infection triggers localized edema - fluid builds inside the appendix - appendix fills with purulent exudate - pressure inside the appendix escalates causing reputure
156
appendicitis's clinical manifestations
- fever - pain - n/v - anorexia - pressure make it better - check for rebound tenderness
157
ascites
fluid accumulation in abdomen: fluid not being held in vascular system
158
encephalopathy:
elevation of ammonia
159
varices
enlarged vessels- risk for rapture: coughing/ vomitting can cause repture
160
diabetes mellitus
glucose intolerance - faulty production of insulin - tissue insensitivey to insulin
161
type 1 diabetes
- IDDM, juvenile - 5% id diabetes cases etiology: - some genetic component (10%) - autoimmune responses to virus patho: - destruction of beta cells - pancreas secretes no insulin - more common in young, thin pt. - life long insulin given
162
type 2 diabetes
- NIDDM, adult onset - 95% of diabetes cases etiology - large genetic component (90%) - obesity: have pt. loose weight and monitor diet patho: - decreased beta cells responsiveness to glucose - can be put on oral hypoglycemias - regulate/ keep sugars in balance
163
prediabetics
- glucose intolerance | - blood sugars elevated but not diabetic
164
secondary diabetes
- drugs - pancreatic trauma - some other chronic illness that damages beta cells
165
clinical manifestations for diabestes
3 P's: - polyuria - polydispia: increased thirst - polyphagia: increased hunger - fatigue - blurred vision - infection prone - abdominal pain - headache - ketosis/acidosis blood sugars above 100
166
diagnosing diabetes
glucose tests - fasting plasma glucose > 126 mg/dl - casual plasma glucose > 200 mg/dl - glucose tolerance test > 200 mg/dl after 2 Hr additional test: glychomoglobin: normal 4% to 6%
167
hyperthyroidism patho
- increased metabolic rate - increased beta receptors - primary: too much TH - secondary: too much TSH
168
hyperthyroidism causes
- autoimmune (graves disease) - goiter - pituitary tumor (secondary) - thyroid CA - overuse of thyroid hormones
169
hyperthyroidism clinical manifestations
Hypermetabolic state - heat intolerance - increased appetite - weight loss - frequent stools - nervousness - tachycardia, palpitations - tremor - heart failure - warm smooth skin - exophthalmos (GRAVES DISEASE)
170
hypoparathyroidism patho
- decrease in PTH - calcium stays in bones - hyperphosphatemia
171
hypoparathyroidism causes
- heredity | - accidental removal of parathyroid during thyroidectomy
172
hypoparathyroidism clinical manifestations
tenany - neruomucular irritability - numbness and tinging of fingers and peri-oral area - muscle spasms - cardiac dysrthythmias - troussa sign - trasric sign
173
SIADH patho
- too much ADH - water retention - hyponatremia - decreased serum osmolality
174
SIADH causes
- tumors - severe stress/ trauma - cerebral hemorrhage - diabetes insidious tx complications
175
SIADH signs and symptoms
- weight gain without edema - dilution hyponatremia - concentrated urine - muscle cramps and weakness - brain swelling, seizures, death
176
traumatic brain injuries (TBI)
- usually caused by sudden and violent blow or just to the head (closed injury) or a penetrating (open injury) head wound that disrupts the normal brain function
177
traumatic brain injuries (TBI) can
bruise the brain damage nerve fibers cause hemorrhaging
178
traumatic brain injuries (TBI) causes
``` falls being struct by against an object motor vehicle accidents sports acitvies intestinal self harm ```
179
traumatic brain injuries (TBI) conditions associated with closed tbi
concussion: momentary interruption of brain function - usually results from a mild blow to the head that causes sudden movement of the brain, disrupting neurologic functioning - may or may not lead to a loss of consciousness - amnesia, confusion, sleep disturbances, and headaches may occur for weeks or months cerebral contusion: bruising of the brain - most often results from a blunt blow that causes the brain to make a sudden impact with the skull coup: initial area where the brain the skull contrecoup: opposite side of brain where it rebounds and impacts the skull - varies in severity depending on the extent of damage and the amount of bleeding - residual effects depend on severity
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transient ischemic attack
- temporary episode of cerebral ischemia that results in the symptoms of neurologic deficits - also called ministries because these neurologic deficits mimic a cerebrovascuale accident (CVA) or stroke except that these deficits resolve within 24 hours (1-2 hours in most cases) - may occur singly or in a series
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transient ischemic attack warning signs
warning sign that a cva may be impending; however, not all cvas are preceded by tia - 1&3 people experienceing a tia eventually have a stroke hold occur within the year
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transient ischemic attack can occur
because of a cerebral artery occlusion, cerebral artery narrowing, cerebral artery injury
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transient ischemic attack additional risk factors
- migranes - smoking - diabestes mellitus - advancing age - inadequate nutrition, hypercholesterolemia, oral contraceptive usage, excessive alcohol combustion, illicit drug use
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transient ischemic attack complications
permanent brain damage injury from falls cva`
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cerebrovascular accident
stroke - an interruption of cerebral blood supply - ischemic damage is permanent
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cerebrovascular accident causes
total vessel occlusion | cerebral vessel rupture
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cerebrovascular accident major types
- ischemic strokes are most common | - hemorrhagic stroke are most fatal
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cerebrovascular accident complications
neurologic deficits and death
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cerebrovascular accident most common in
african americans and those living in the south east region
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cerebrovascular accident additional risk factors
``` physical inactivity phychosocial stress obesity hypertension smoking dyslipidemia diabetes mellitus atherosclerosis oral contraceptive usage excessive alcohol combustion illicit drug use advancing age ```
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cerebrovascular accident treatment
- requires prompt treatment to minimize brain damage - determining whether the cva ischemic or hemorrhagic on origin prior to treatment - treatment should be delivered within 3 hours of symptom onset
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osteoporosis
hip/ vertebral fractures - reduced quality o lie - increased liability - risk of death (during year after fracture)
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osteoporosis prevention
- build bone through age 30 - obtain adequate calcium and vitamin d - exercise (especially childhood) - avoid alcohol and smoking - fractures can be life treating - increased rate of death in first year over age 50
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osteoporosis risk factors
- female gender - aging - causcasins - asian - smal boned, petite - postmenopausal status - low testosterone and estrogen in men - family history - history of fractures - low calcium intake - low vitamin d - excessive caffein, protein, sodium - sedentary lifestyle - excessive alcohol use - cigarette smoking
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fractures
breaks in bones - open- break skin - closed- does not break skin - complete: done divided into 2 or more pieces - incomplete: no degree of separation
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fracture cause
trauma | pathological
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simple fracture
clean break | maintain of alignment
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communuted fracture
multiple fractures
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spiral fracture
twist around bone shaft
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fracture healing process
1. clot formation at fracture site 2. fibroblast and osteoblast arrive, fibrocartilage callus forms 3. new bone forms 4. bone remodeling continues until bone intact, repair and healing completed takes up to 4-6 weeks
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pressure injuries
- soft tissue injuries that result of unrelieved mechanical pressure - results in areas of necorsis and ulceration where the tissue is compressed between bony prominences and extrernal hard surfaces - can develop in 1-2 hours if pressure is not relieved - classification using a stagng system but not all injuries follow a linear progression
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pressure injuries common sites
``` sacrum ischial tuberosities trochanters malleoli heels can develop anywhere ```
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pressure injuries risk factors
``` advancing age impaired circulation tissue perfusion immobilization malnutriton decreased sensation incontinence ```
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stage 1
skin is intact, nonblanchable erthema is present
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stage 2
erosion or blister with or without true ulcerations, no exposed sub c tissue
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stage 3
full thickness skin loss with damage to sub q tissue down to the underlying fascia
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stage 4
full thickness skin loss with extensive destruction, tissue necrosis, and damage to exposed supporting structures
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deep tissue injury
skin may or may not be intact | underlying tissue is damaged
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unstageable
full thickness skin tissue loss in which the extent of damage cannot be determined because it is hidden by slough or eschar
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pressure injuries complications
challenging mitigating factors - ulcers can become infected with hospital acquired - antibitoic resistant organism - sinus tracts - osteomyelitis - cellutitis - tissue calcifcation - bactermia - meningitis - endocaridits - squamous cell carcinoma
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pressure injuries diagnosis
physical examination | additional test depending upon the stage
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pressure injuries treatment
``` reduce pressure care for wound minimize infection support nutritional needs pain management antibiotics negative pressure therapy topical recombinant growth factors electrical stimulation therapy therapeutic ultrasonography surgical closure skin grafts ```
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pressure injuries healing
take weeks, prevention is critical several scales developed to assess risk: - norton scale - braden scale
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viral infectons: herpes zoster (shingles)
- caused by the varicella-zoster virus - appears in adulthood years after primary infection of varicella in childhood - virus lies dormant on a cranial nerve or a spinal nerve dermatone untill it is activated years later - virus affects this nerve only, giving the condition its typical unilateral manifestations
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herpes zoster (shingles) manifestations
- pain - paresthesia - red or silvery vesticaulr rash develops in a line over the area innervated by the affected nerve (may last for weeks or months) - extremely sensitive skin - pruritis
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herpes zoster (shingles) complications
neuralgia and blindness
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herpes zoster (shingles) treatment
antivirals antidepressants anticonvulsants vaccines
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abnormalities of urethral meatus
epispadias | hypospadias
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epispadias
dorsal (upper) opening
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hypospadias
ventral (underside) opening
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cryptorchisim
one or both testes undescend - prior to birth - common birth defect - right more than left - 80% naturally descend - after 6 months see a doctor
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erectile dysfunction
known as impotece etiology: - physchological: stress, depression, relationship issues, smoking, obesity, medications - neurologic- spinal cord injuries - vascular-cardiovascular impairment, HTN, DM, asclerosis
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priapism
prolonged erection > 4 hr typically painful patho: - blood cannot drain from penis --> ischemia--> tissue damge etiology: - age: 5-10 20-50 - blood, circulatory, nervous dysfunction - sickle cell, leukemia, trauma, tumors, DM, MS, stroke, medications, alcohol, drug use
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hydrocele
- fluid in scrotal sac= enlargement of scrotum - uncomferable etiology: - congenital - inflammation, infection, trauma
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varicocele
- dilation of a scrotal vein --> painful swelling - most commonly affects left testicle etology - congenital - obstruction
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testicular torsion
twisting of the testes and spermatic cord
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prostate cancer
- most common cancer among men - minimal metastasis: 90% localized - enlargement of prostate: compression of urethra risk factors: - family hx - sti - inherited genetic conditions
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testicular cancer
- men 15- 34 years old - often asymptomatic - usually affects one testicle: hard painless mass, testicle enlargement, gynecomastia
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testicular cancer risk factors and prevention
- family hx - infection - trauma - alcohol use - cryptochidism prevention: - early detection --> self testicular exam
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amenorrhea
absense of mestruation primary: - females >16 have yet to start menstruation secondary: - changing hormone levels: tumors, weight loss, chemo, eating disorders
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dysmenorrhea
painful menstruation | - affects the ability to complete daily activites
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cystocele
bladder sags into vaginal space | - urinary freqeuncy and or incontinence
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rectocele
portion of rectum sags into vaginal space | - constipation, soiling, or painful defecation
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uterine prolapse
uterus sags into vaginal space | - fullness within the pelvis, backaches, and stress incontinence
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patho of pelvic organ prolapse
heavy lifting, constipation and obesity
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endometriosis
functioning tissue cyclically sloughs off patho: - functioning tissue thickens, slough and bleeds like normal endometrial tissue - blood becomes trapped -->irritation, pain, scaring, and adhesions etiology: - unclear
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endometriosis risk factors
- early onset mestruation - late onset menopause - delayed childbearing or nulligravida
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breast cancer
- cancer in glandular tissue of the breast risk factors - early menses - nulligravida - last menopause - familt hx - genetic predisposition: brca gene prevention - monthly breast self exam
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cervical cancer
- cancer of the cervix - 100% survial rate w/early detection etiology: HPV screening: pap spear prevention: HPV vaccine
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endometrial cancer
cancer of endometrial tissue: uterine linning - 83% 5 year survial rate - etology unknown risk factors: - excessive estrogen - obesity - inactivity - htn
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ovarian cancer
cancer of one or both ovaries - 47% 5 year survival rate: no screening tool risk factors: - genetic predisposition: BCRA - early menses - late menopause - excessive estrogen - obesity
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STI
transmission - sexual contact - mother to child: preg/childbirth - blood incidence rate - 20 million new STI in 2019 15-24 years mandated reporting: - chlamydia - gonorrhea - syphillis
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chlamydia
etilogy: chlamydia trachomatis transmission - sexual contact - mother to child during childbirth incubation - 1-3 weeks treatment - antibiotics: 7 days
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genital herpes
etiology: herpes simplex virus (HSV) 1. type 1- above wait cold sores 2. type 2- below waist transmission - sexual contact - oral- genital contact - mother to child (type 2 only) incubation - 4 phases - lifelong recurrence treatment - antivirals
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genital warts
etiology - human papillomavirus - affects 79 million transmission - skin to skin contact - mother to fetus prevention - hpv vaccine
patho
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