Emma Pathophysiology

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This set includes various questions regarding Pathophysiology in Nursing

an adaptive cell response that could be a precursor to cancer is

dysplasia

the most frequent source of free radicals in the body is

oxygen
the best way to rid the body of free radicals is antioxidants
free radicals are cell particles which have an impaired electron

impaired wound healing may be due to

lack of vitamin C, hypoxia, corticosteroid therapy, lack of vitamin A

a benign tumour of glandular tissue is called

adenoma

neoplasia results when

cell differentiation and growth characteristics become altered

what features apply to malignant but not benign tumours

grows at the periphery and infiltrates surrounding tissue

what are the steps of metastasis is the correct order

-break loose from the primary tumour
-invade surrounding extracellular matrix
-gain access to and survive in the bloodstream
-emerge from blood and invade surrounding tissue

which of the following is NOT one of the american cancer society's 7 early warning signs of cancer

IS:
-a nagging cough
-a sore throat that does not heal
-a change in a wart or mole

ISN'T:
-a sudden decrease in hearing

oncogenesis is best described as

genetic mechanism whereby normal cells are transformed into cancer cells

the human immunovirus (HIV) is transmitted in all of the following ways except

IS:
-perinatally
-sexual contact
-blood contact

ISN'T:
-casual contact

seroconversion i.e. when HIV antibodies can be detected in the blood following exposure typically takes

3 months

which one of the following statements is true (about HIV)

FALSE:
-an HIV-infected person can transmit the virus to others before seroconversion

TRUE:
-an HIV-infected person can not transmit the virus to others before seroconversion
-an HIV-mother will not infect her infant with HIV through breastfeeding
-in healthcare workers the occupational risk of HIV infection is greater than for Hepatitis B infection

the most common opportunistic infection occuring in persons with AIDS is

pneumocystis carinii

a deficiency is B lymphocytes will cause reduced levels of

antibodies

which one of the following is NOT part of the acute inflammatory response

IS:
-chemotaxis by mast cells
-phagocytosis by neurophils
-activation of complement

ISN'T:
-formation of granulomas

_________ are the predominant phagocytic cell early in the immune response

neutrophils

which of the following hypersensitivity reactions does not involve antibody

type IV (4)

odema due to increased capillary pressure can occur with

heart failure

accumulation of fluid in the abdominal cavity is termed

ascites

dehydration of the elderly commonly occurs for all of the following reasons EXCEPT

IS:
-a decrease in the ability to sense thirst
-decreased sensory ability following stroke
-confusion and loss of short term memory

ISN'T:
inceased sensation with electrolyte imbalance

increased levels of antidiuretic hormone are associated with

nausea

raised levels of aldosterone could lead to

hypokalaemia and hypernatremia

decreased fluid intake and dehydration is likely to manifest as

weight loss

decreased intestinal absorption of vitamin D, eg. following surgical resection of part of the intestine, can result in

hypocalcemic tetany

hyperparathyroidism leads to

elevated serum calcium levels

the major protein buffers in the vascular compartment are

albumin and plasma globulins

which acid-base imbalance would have a deficiency of bicarbonate

metabolic acidosis

prolonged tissue hypoxia following caridac arrest and resuscitation would be expected to cause

metabolic acidosis

prolonged bladder outflow obstruction from prostatic hypertrophy can result in

-urinary stasis
-stone formation
-dilation of ureters
-hydronephrosis

what is the correct order for the progressive stages of renal failure

(ESRF: end stage renal failure)

-diminished renal reserve
-renal insufficiency
-renal failure
-ESRF

arterial pressure increases if

peripheral resistance increases

a __________ aneurysm develops when an inner arterial layer tears and blood forces it's way between arterial wall layers

dissecting

if a thrombus in the L) common iliac vein became dislodged which arteriole system would it enter first

lungs

the pain associated with angina is due to

ischaemia of the myocardium

loss of the sympathetic nerve supply to the heart would result in

decrease in heart rate

the symptoms of weakness and east fatigability in persons with congestive heart failure (CHF) are probably a consequence of

low cardiac output

which one of the following arrhythmias is usually fatal without prompt treatment

ventricular fibrillation

what correctly depicts the functional difference between the L) and R) heart of a person with chronic obstructive respiratory (pulmonary) diease

the R) heart works against greater resistance than the L) heart

the pathological changes associated with chronic bronchitis include

hypertrophy of the bronchial glands

in bronchial asthma when there is exacerbation

medium and small sized bronchi are plugged with mucus

a rise in the carbonic acid levels of blood will affect respiration in which way

the respiratory rate increases and the breathing becomes stronger and deeper

the primary ventilatory problem associated with obstructive lung disease such as exacerbation of COR/COPD or asthma is

delay of the airflow out of the lungs

a person who has COR pulmonale will have

right heart hypertrophy

a person who has respiratory insufficiency could be expected to have

pH below normal

the pulmonary oedema associated with adult respiratory distress syndrome (ARDS) is caused by

increased membrane permeability

which condition is commonly associated with haemoptysis

pulmonary tuberculosis

in early hypovolaemic shock a reduction in the circulating blood volume would give risk to

narrowing of the pulse pressure

in disseminated intravascular coagulation (DIC) there is

sluggish tissue flow causing agglutination and microclot formation

vascular disease of the lower limb - cool to touch and with pain relieved by dependant position - is most likely due to

artherosclerosis

why are venous thrombi more common than arterial thrombi

aterial flow and pressure are lower in veins

risk factors for venous thrombosis

-ageing
-inactivity
-dehydration
-hypercoagulability
-increased hematocrit
-constrictive clothing

what are the clinical manifestations of venous thrombosis

-pain
-tenderness
-redness and swelling over the area of the thrombus
-some people have no symptoms

the major complication of deep vein thrombosis (DVT) is

pulmonary embolus

what is an allergen

antigens that induce exaggerated immune responses

when discussing allergic reactions to bee stings, what are the underlying mechanisms that trigger Type 1 immune responses in the body

type 1 responses mediated via IgE antibodies that bind to mast cells (or other immune cells) triggering the release of histamine and other inflammatory mediators

examples of clinical manifestations that may occur in allergic reactions are

GI:
-vomiting
-abdominal pain
-diarrhea
SKIN:
-urticartia
-itching
-angioedema
-conjunctivitis
RESPIRATORY:
-bronchospasm
-rhinitis (irritation and inflammation of the mucous membrane inside of the nose)
-asthma
-laryngeal oedema
CV:
-hypotension
-tachycardia
-arrhythmia
-vasodilation

how may emphysema occur in persons who are not exposed to cigarette smoke

inherited deficiency of alpha/antitrypsin
an enzyme that inhibits proteolytic destruction of lung tissue

persons with CORD/COPD should not receive oxygen therapy via tightly fitting face masks, what is the physiological reason for this

normally central chemoreceptors near the respiratory centres in the medulla are stimulated by increased PaCO2 (which reduces pH or raised carbonic acid)
chronic hypercapnia desensitizes central chemoreceptors and persons affected rely on peripheral chemoreceptors that respond to hypoxia
high levels on inspired oxgen inhibit peripheral chemoreceptors

what is idiopathic

of unknown cause

CVA stands for

cerebrovascular accident (stroke)

what are free radicals

cell particles which have an unpaired electron
unpaired electrons can attach to other
cells causing instability and agitation to other cells

define necrosis

changes that follow cell death in living tissue
progressive degradation of enzymes on the lethally injured cell
appearance of necrosis is the result of enzyme disgestion and denaturation of proteins

oxidative stress

characterised by an imbalance between the levels of damaging reactive free radicals and the antioxidant defense mechanisms present within cells

apoptosis

a process of programmed cell death of single cells scattered in a population of healthy cells

what is cancer

cancer is an abnormal multiplication of cells

classification of cancer includes

-cell type
-degree of differentiation
-malignant/benign
-location
-spread

carcinogenesis is

the transformation of a normal cell into a cancer cell

angiogenesis is

formation/production of new blood cells

carcinogens are

agents that bind to DNA => cell mutations acts as initiators/promoters eg.:
-industrial agents
-aniline dyes
-heavy metals
-asbestos
-benezenes
-soot
-cigarette smoke
-charcoal
-aflotoxins
-x-ray
-ultra violet rays
-microwave
-gamma rays

what is hyperplasia

cells in a tissue overgrow resulting in a defined mass (tumour/neoplasm)
is benign (eg. moles)
has a slow growth rate
expands in the same tissue
often in response to hormonal stimulation

what is dysplasia

an abnormal change in the size, shape, and organisation of cells in a tissue
often an early step towards cancer
microscopic characteristics of cancer cells
behave differently from normal cells

deranged cell growth of a specific tissue
variation in size, shape and loss of cell orientation with alteration in nucleus
potentially reversible if not too severe
BUT: can go on to become cancer
grades of change: 1, 2, 3 can go on to become carcinoma in situ (CIS)

in cervical cancer:
cells become increasingly displasic => low grade changes CIN1 => CIN2 can go on to become high grade => CIN3 => CIS

peripheral vascular disease (PVD) includes

-aneurysm
-primary varicose veins
-venous thrombosis (thromboembolus)

what are the 3 types of myocardial ischaemia

-stable
-variant
-silent

myocardial ischaemia : stable

due to atheroma
comes on with increased muscle contraction resulting in lactic acid
pain may be referred
associated with a stable plaque

myocardial ischaemia : variant

coronary artery spasm
comes on at rest
? due to sympathetic activity or decreased prostaglandins

myocardial ischaemia : silent

no angina pain
may have dyspnea and fatigue
more common in women

what is myocardial ischaemia

the lack of/little blood supply to the myocardium, the heart muscle
lack of O2 to muscles and tissues of heart, specific area only

what is coronary heart disease

the narrowing or blockage of the coronary arteries that supply blood and oxygen to the heart
usually caused by atheroscelrosis
telemetry is cardiac monitoring

urinary tract obstruction

an interference with the flow of urine at any site along the urinary tract
the obstruction can be caused by an anatomic or functional defect
lower urinary tract symptoms:
-tumours
-strictures
-calculi
-benign prostate hypertrophy
upper urinary tract symptoms:
-stones
-tumours
-enlarged lymph nodes
-polycystic kidney disease
severity is based on:
-location
-completeness
-duration
-involving one of both upper urinary tracts

glomerular disorders

mostly result of immune dysregulation
results in sudden on insideous onset of hypertension, oedema and an elevated blood urea nitrogen (BUN)
decreased glomerular filtration rate
elevated plasma creatinine, urea and reduced creatinine clearance

glomerular damage

PROLIFERATIVE: number of cells increase
SCLEROTIC: amount of extracellular matrix increases
MEMBRANOUS: thickness of glomerular capillary wall increases
all can decrease the efficiency of filtration
allow blood cells, lipids, or proteins to pass into the urine

what is the definition of obesity

excess body fat caused by the energy intake exceeding the energy output of the body over an extended period of time

obesity complications

insulin resistance in type 2 diabetes: high fasting sugars and increased triglycerides
CV disease: dyslipidaemias, hypertension, CHD, CH, stroke etc
cancer: bowel, breast, ovary
gallstones: fatty, liver and in females
arthritis: esp. weight bearing joints
dyspnea: SOBOE then at rest, excess weight need more oxygen and lung expansion is decreased
snoring
obstructive sleep apnea due to decreased airways and decreased lung expansion which can lead to deacreased PO2 and hypoxaemia
excessive sleepiness
irritability
psychosocial problems
infertility

what are the four cardinal signs of acute inflammation

redness (rubor)
heat (callor)
swelling (tumor)
pain (dolor)
+ loss of function (functio luefa)

inflammation response

begins with a flood of inflammatory chemicals released into the extracellular fluid
includes kinins, prostaglandins, complement and cytokines which are released by injured tissue, phagocytes, lymphocytes and mast cells
causes local small blood vessels to dilate resulting in hyperemia

inflammation response : vascular permeability

chemicals liberated by the inflammatory response increases the permeability of local capillaries
exudate (fluid containing proteins, clotting factors, and antibodies)
seeps into tissue spaces causing local oedema (swelling) which contributes to the sensation of pain
IgE : trigger immune response, stops the response of histamine

inflammatory response : oedema

the surge of protein-rich fluids into tissue space (oedema):
-helps to dilute harmful substances
-brings in large quantities of oxygen and nutrients needed for repair
-allows entry of clotting proteins, which prevents the spread of bacteria

inflammatory response : phagocytic mobilisation

occurs in four main stages:
leukocytosis : neutrophils released from bone marrow in response to leukocytosis - inducing factors released by injured cells
margination : neutrophils cling to walls of capillaries in the injured area
diapedesis : neutrophils squeeze through capillary walls and begin phagocytosis
chemotaxis : inflammatory chemicals attract neutrophils to the injury site

inflammation versus infection

inflammation involves non-specific immune responses to cell injury
it happens the same regardless of the cause
infection : from invasion of micro-organisms, causes cell injury and inflammation
can have inflammation with/without infection, infection is from pathogens

atrophy is

shrinking in cell size resulting in decreased size of a body part
causes include:
-disuse
-deneruation
-ischaemia
-poor nutrition
-often reversible

hypertrophy is

an increase in cell size resulting in increased size of a body part
may be physiological
eg. with resistance training
may be pathological
eg. heart ventricle muscle with heart failure

metaplasia is

fully differentiated adult cell converts to another cell type in response to stimulus
eg. in smokers airways chronic irritation => ciliated epithelium replaced by more robust stratified squamous epithelium

when a cell changes from one type to another
not definite cancer

tuberculosis is

infectious disease due to myocobacterium tuberculosis (human or bovine form)
spread via droplets, infects lungs and occasionally GI tract
inhaled bugs multiply, affecting alveoli in upper lobes, some escape to lymph nodes and set up immune responses
inflammation occurs within hours, neutrophils surround organisms
after a few days macrophages surround organisms

asthma is

a chronic inflammatory disease of airways involving mast cells, eosinophils, T cells, neutrophils, macrophages and epithelial cells (+++)
it causes recurrent episodes of wheezing and coughing often during the night
often reversible : spontaneously or with treatment
inflammation causes bronchial hyper-responsiveness to a variety of stimuli

asthma pathophysiology

triggered by allergens or irritants exposed to hyper-responsive airways
IgE and mast cell degranulation release
inflammatory mediators and chemotaxis attracts WBC
resulting inflammation causes bronchial smooth muscle spasm, increased vascular permeability and mucus, vascular congestion, oedema, thick sputum, eventually thickening airway walls

atelectasis is

collapse of lung tissue (alveoli)
two types : compression and obstruction (absorption)
compression : pressure on part of a lung eg. from tumor, fluid, air in pleura or abdominal distention
obstruction (absorption) : eg. from a mucus plug, inhaled anaesthetics => absorption of distal alveolar air and collapse
risk increases with pain, ineffective airways clearance post-operatively

bronchiectasis is

irreversible dilation and destruction of bronchial walls
caused by:
-repeated respiratory infections (common)
-tumor obstruction
-apsirated FB (?)
-congenital (rare)

COPD

chronic obstructive pulmonary disease
chronic bronchitis - inflammation and irritation of airways
emphysema - destruction of the alveoli and surrounding capillaries with a reduction in areas for gas exchange

chronic bronchitis

associated with irritants in airways - smoking
middle aged men most commonly affected
excessive mucus production of irritated airways mucosa causes recurrent infections
chronic productive cough for 3 consistent months of the year, (3/12) for at least 2 consecutive years
pulmonary hypertension and right heart failure follow with peripheral edema
narrowed airways collapse causing air trapping => hypoventilation => hypercapnia

emphysema

enlargement and destruction of airspaces distal to terminal bronchioles (+++)
pan-lobular : affects peripheral alveoli
centrilobular : affects respiratory bronchioles with initial preservation of alveolar ducts and sacs
emphysema causes alveolar air trapping dyspnea, altered V/Q, increased ventilatory effort

cystic fibrosis

a heredity autosomal recessive disease
thick tenacious mucus in resp tract
have chronic respiratory disease, from hyperplasia of goblet cells, viscid mucus plugs => bronchial obstruction => inflammation, repeated infections, bronchiectasis, hypoxaemia and clubbing => pulmonary hypertension => eventually rheumatic heart failure at a young age
diagnosis: Guthrie test, increased sodium chloride (NaCI) in sweat, early treatment essential to avoid death in childhood

cardinal signs of respiratory disease

cough : responds to irritants (increased sputum)
sputum : clear, purulent
dyspnea : graded 0-4
orthopnea : SOB lying flat

hypoxaemia

decreased O2 transported in blood
eg. pneumonia
airway obstruction
shallowing breathing eg. abdominal ascites

hypoxia

reduction in tissue oxygenation
caused by: an increased altitude
sudden blood loss
acute circulatory or respiratory problems
severe hypoxia : PO2 < 60 mmHg

hypercapnia

increased CO2 in arterial blood
caused by decreased drive to breathe or inability to respond to ventilatory stimulation eg. airway obstruction
respiratory depression, decreased nervous stimulation of respiratory muscle, damage to brain stem, increased work of breathing

circulatory shock

a clinical syndrome characterised by decreased cardiac output, failure of the circulation, inadequate tissue perfusion and hypoxic cellular damage that results in impaired cell functioning which can go on to cell death, organ dysfunction and stimulation of inflammatory responses

types of shock

hypovolaemic : loss of at least 15% of circulating blood volume
obstructive : (cardiogenic) reduced cardiac output
distributive : loss of vasomotor tone
peripheral pooling
septic (endotoxins)
failure of cells to take up oxygen

arterial varicose veins

caused by:
incompetent valves meaning blood won't get to the limbs
this can also cause ulcers and itching etc
manage by:
increased exercise, increases circulation and increases the ulcer status

venous varicose veins

caused by:
incompetent valves meaning blood can't get away from the limb back to the heart
manage by:
elevating legs to encourage blood flow

prinzmetal

a type of MI (myocardial infarction)
variant angina
causing spasms
doesn't require immediate attention
occurs at rest
often is what patient may show with MI

what is PO2

partial pressure of oxygen

what is ischaemia

lack of blood supply, causing no O2 getting through body, causing hypoxia

anaplasia is

definite cancer

inflammatory responses vascular and cellular

IMMEDIATELY: haemostasis vascular constriction and clotting contain wound: form surface scab
then: increased capillary permeability => leakage of plasma and blood components to exit vessels
followed by cellular effects of WBC and phagocytosis
initially phagocytosis by neutrophils, then macrophages: remove debris, bugs, etc. WBC release growth factors (GFs) => angiogenesis (new capillaries) and attract fibroblasts
is non-specific
increased WBC, neutrophils in WBC
neutrophils are main WBC in inflammation, have a phagocytic response

carcinogenesis

risk/contribute factors increased risk of cancer: - oncogenic viruses, chronic inflammation, chemical and environmental carcinogens, heredity, altered immunity
some diseases can have a carcinogenic effect on the tissues
increased risk = oncogenic viruses

oncogenesis

2 week process: needs something to trigger it and something to promote it
hormones can induce cell mutations of act as promoters
eg: cervix cancer resulting from HPV virus that is then promoted by hormones leading to cancer

oncogenic viruses

virus DNA replaces the cells normal DNA and then multiplies

carcinogens

agents that bind to DNA causing cell mutations that act as initiators/promoters and take over

solar ionising radiation and physical agents

damage DNA - mutate proto-oncogene or inactivate tumour suppressor gene
sunlight with UV radiation
EMF controversial
chronic irritation could promote it eg. jagged teeth, pipe, can cause oral cancers eg. leukoplakia
alters normal DNA, becomes dysplasic, later turning cancerous

metastases: steps

angiogenesis and tumour growth, attachment to basement membrane, invasion and enzymatic breakdown of membrane, increased motility and detachment, dissemenation in blood, lymph etc, survival from immune cells, mechanical entrapment or adhesion, extravasation, growth at 2o site?

4 types of hypersensitivities are

Type I: E mediated
Type II: bacteria in wound
Type III: immune complex-mediated: virus
Type IV: anaphylaxis (IgE)
for hypersensitivity to occur you need an antigen to trigger the response
antibodies are soluble proteins secreted by activated B cells and plasma cells in response to an antigen

classes of antibodies include:
IgB: B cells
IgM: plasma cells
IgA: epithelial
IgE: mast cells, basophils

hypersensitivity reactions: type I

IgE binds to mast cells causing release of histamine and other inflammatory substances
response is immediate, usually localised and subsides in 30 mins
manifestations seen is skin, respiratory tract, GI tract eg. ASTHMA, hay fever
systemic responses are rare when allergens enter blood - anaphylaxis

hypersensitivity reactions: type II

mediated via IgG or IgM
onset 1-3 hours, lasts 10-15 hours
antibodies bind to tissue specific antigens
this triggers complement or phagocytosis by macrophages (or neutrophils) or non-specific cell destruction by cytotoxic T cells or receptor blockage
eg. some drug and transfusion reactions

hypersensitivity reactions: type III

IgM or IgG mediated
soluble antigens widely distributed - antigen antibody complexes
complement activated: attracts neutrophils, attempt phagocytosis, immune complexes too big => inflammation persisting in a particular area causing tissue damage; eg mushroom growers or pigeon breeders alveolitis

hypersensitivity reactions: type IV

delayed hypersensitivity; 1-3 days
mediated by sensitised T cells
involves cytotoxic Ts, T helpers, macrophages (release cytokines directly attack target cells)
eg. allergic contact dermatitis, latex allergy, plant allergies, mantoux test, can be transferred by transfusion
antihistamines don't work, steroids do on cytokines

lipoproteins

cholesterol/triglycerides carried in plasma by fat-transporting proteins (apoproteins)
5 types, classified by densities
carry varying amounts of triglycerides, cholesterol, phospholipids
apoproteins control interactions of lipoproteins
chylomicrons: transport dietary lipids from the intestines to other locations in the body
LDLs: BAD
HDLs: GOOD : carry excess cholesterol from the arteries to the liver to be made into bile

atheroclerosis

deposits of fat and fibrin on endothelium of arteries that hardens over time eventually => decreasing lumen size
affected arteries = medium and large arteries eg. aorta and its branches, coronary and cerebral arteries
insidious: 20-40+ years => symtpoms
endothelium: allows for exchange and extra fat absorption
reversible at fatty streak stage, early stages (usually seen in children)

hyperlipidaemia

elevated cholesterol levels increase risk of atherosclerosis
dyslipidaemias: high LDLs, high total cholesterol, low HDLs
increased cholesterol from genetics, nutrition, disease, lifestyle

peripheral vascular disease

any condition that impairs peripheral circulation, aterial or venous
aterial: atherosclerosis: occlusion from thrombus/embolus, commonest lower limbs: aorto-iliac, femoro-popliteal, popliteal-iliac arteries
narrow lumen => ischaemia, pain at rest, intermittent claudication, decreased foot pulses, cool, elevate limb => pallor

acute coronary syndromes

term for unstable agnina, MI without ST elevation, MI with ST elevation
plaque starts to fissure, clot begins to form, breaks up, still have flow to myocardium
unstable angina: presents 3 ways:
prolonged symptoms at rest
severe new onset stable angina
worsening stable angina
pre-infarction state: clot can grow=> obstruction

where is the most common site of an MI

left ventricle

clinical manifestations of MI

prolonged O2 deficit => ischaemic death of heart muscle at same time end products of anaerobic metabolism accumulate
chest pain may be referred
sympathetic effects: nausea and vomiting, pallor, diaphoresis, tachycardia, anxiety, restlessness, sense of impending doom
DP drops/unchanged
up to 50% silent infarcts
diagnosis confirmed with enzyme changes
CK (creatinine kyamine) energy transfer enzyme, 4-6 hours, peaks 18-24 hours
troponin I: relaxing protein, released in hours, peaks 1-2 days
ECG

HIV pathophysiology

HIV retrovirus (genetic info is in RNA) - slow virus: long delay from infection to symptoms
targets cells with CD4+ receptors in immune nervous systems (T helpers, macrophages, dendritic cells) (+++)
viral envelope has protein spikes: GP120 that interact with receptors of target cells, cause a conformation change and allow the viral core into the host cell
there may be a long time between the exposure and expression of symptoms

HIV inside the host cell

the HIV uses reverse transcriptase to convert its RNA to 2 stranded DNA
a 2nd enzyme helps this DNA into host cell DNA
infected cells may remain dormant
once activated, this DNA reprograms host cell DNA to make viral protein: assembled and coated in cytoplasm, then bud off as new virions and finally host cell dies

HIV transmission of infection

directly through infected body fluids
unprotected sexual intercourse
healthcare workers (needle sticks)
sharing needles
blood transfusions/products
maternal
cadaver

clinical manifestations of HIV (+++)

early stage: symptoms similar to flu eg:
night sweats
lymphadenopathy
fatigue
malaise
without treatment, immunity declines
progresses from HIV to AIDS (read how this happens)

CRF definition

chronic renal failure: permanent loss of nephrons and renal function

erythropoietin definition

hormone produced by kidneys and regulates production of red blood cells

filtrate definition

liquid entering the nephron

filtration definition

movement of liquid through a membrane (like a sieve), allows only small molecules and liquids to pass through
movement is from higher to lower pressure

GFR definition

glomerular filtration rate: amount of filtrate produced each minute

glomerulus definition

filtration system of the nephron, composed of capillaries surrounded by a thin double-walled capsule, called Bowman's capsule

renal physiology

-control the fluid/electrolyte balance for the body
-remove metabolic wastes from the blood and excrete them to the outside
-regulate red blood cell production
-regulate blood pressure
-important in calcium ion absorption
-control volume, composition and pH of the blood

glomerular disorders

glomerular disease mostly the result of immune dysregulation
results in a sudden or insidious onset of hypertension, edema, and an elevated blood urea nitrogen (BUN)
decreased glomerular filtration rate - elevated plasma creatinine, urea and reduced creatinine clearance

nephritic syndromes

glomerular disorders that INITIATE THE INFLAMMATORY RESPONSE within the glomeruli and initially DECREASES permeability of the membrane

nephrotic syndromes

glomerular disorders that affect the glomerular capillary membrane and INCREASE permeability to plasma proteins

glomerular damage

proliferative: number of cells increase
sclerotic: amount of extracellular matrix increases
membranous: thickness of glomerular capillary wall increases
all can decrease the efficiency of filtration
allow blood cells, lipids or proteins to pass into the urine
when there is glomerular damage, blood is passed into the urine (haematuria)

further causes of obstructive shock include

heart prevented from pumping
see renal heart failure and increased cardiovascular pressure (CVP)
PE- pulmonary edema
tension pneumothorax

compensatory mechanisms of shock

body attempts to restore tissue perfusion and oxygenation in early stages of shock with neuro-endocrine and smooth muscle responses
for clinical assessment and treatment shock is divided into 3 stages:
compensated
progressive
decompensated/irreversible
in reality, shock is a continuum

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