Save
Upgrade to remove ads
Busy. Please wait.
Log in with Clever
or

show password
Forgot Password?

Don't have an account?  Sign up 
Sign up using Clever
or

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
Your email address is only used to allow you to reset your password. See our Privacy Policy and Terms of Service.


Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.
focusNode
Didn't know it?
click below
 
Knew it?
click below
Don't Know
Remaining cards (0)
Know
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

BONUS:

other questions:

QuestionAnswer
morula 16 cells in a solid ball of cells (blackberry) made at day 4 after zygote divides
early blastocyst morula with a big hole in the middle
late blastocyst blastocyst but it begins to make differentiated layers eg trophoblast and embryoblast
LHF problem emptying blood into the aorta (LVF/systolic) or filling properly (diastolic). Leads to blood backing up into lungs, causing pulmonary edema (symptoms dyspnea, crackles, pink frothy sputum, paroxysmal nocturnal dyspnea). Most common type.
RHF problem pumping blood into lungs leading to blood backing in systemic venous system causing prominence of internal jugular veins (JVD) and dependent pitting oedema in legs ankles etc
systolic heart failure heart cannot pump properly characterised by a low ejection fraction (EF <40%/ 50%)
diastolic heart failure heart cannot fill properly characterised by a normal or preserved ejection fraction (EF > 60%) at rest often due to a stiff ventricle
most common cause of diastolic HF concentric LV hypertrophy due to essential hypertension
EF = SV / EDV
normal EF range 55-80%
BNP B-type natriuretic peptide (cardiac neurohormone secreted from ventricles in response to volume overload and SNS activation causing VASODILATION via natriuresis/ diuresis
key diagnostic tests for heart failure N-terminal pro BNP, 12-lead ECG (shows LV hypertrophy, electrical issues) Transthoracic Echocardiogram (TTE) - shows if it's systolic or diastolic failure, and assesses EF. CXR - for visualizing pulmonary edema.
S3 heart sound normal in young people BUT in young adults it often indicates volume overload eg in systolic heart failure
S4 heart sound ALWAYS PATHOLOGICAL indicating stiff ventricle eg in diastolic HF
MCMV means tells average volume (size) of RBC
MCV formula haematocrit / RBC count
pre-embryo stage/ germinal period first 2 weeks (where zygote undergoes cleavage, morulation, and blastulation)
embryo stage weeks 3-8 (gastrulation and formation of germ layers and major organ systems)
foetus stage week 9 onwards (organs mature and fetus grown significantly beginning to look more human like)
inner cell mass of blastocyst embryoblast (makes embryo proper)
outer cell layer of blastocyst trophoblast (gives rise to placenta)
basophils blueberries (purple and in anaphylaxis releasing heparin and histamine)
eosinophils raspberries (pink and in allergic inflammation)
difference between ionotropic and chronotropic ionotropic is contractions and chronotropic is heart rate
BP formula CO X total peripheral resistance
where is the needle injected in thorax for samples close to upper border of lower rib in intercostal space 9 in midaxillary line
triangle of safety for chest tube insertion formed of (3) lateral border of pectoralis major anteriorly, lateral border of latissimus dorsi posteriorly, and inferior horizontal line from nipple (5th intercostal space)
typical thoracic vertebrae 2-8
atypical thoracic vertebrae 1st and 9-12
where does the pectoralis major insert into intertubercular (or bicipital) groove of the humerus
which nerve innervates the pectoralis minor muscle medial pectoral nerve (C8, T1)
which nerve innervates the pectoralis major muscle medial and lateral pectoral nerve
sternocostal head of the pectoralis major attaches to the sternum and upper 6 costal cartilages
clavicular head of the pectoralis major attaches to the medial half of the clavicle
attachments of the pectoralis minor muscle Coracoid process of scapula to ribs 3-5 near cartilage
pectoralis major movement at shoulder joint adduction and medial rotation
costochondral joint type of joint synchondrosis joint
origin of the intercostal muscles lower border of the rib above. This allows them to act on the rib below.
What makes up the manubriosternal joint symphysis - secondary cartilaginous joint.
Flail chest means 3 or more adjacent ribs are fractured in multiple places, leading to a segment of the chest wall that moves paradoxically (inward on inhalation, outward on exhalation)
most effective way for detecting IgE-mediated type I allergic reactions. skin prick test
when you get a positive skin prick test, what two things would you typically observe at the site where the allergen was applied wheal (a raised bump) and a flare (redness around the bump)
IgM-mediated Type II HSR works by causing lysis via the membrane attack complex (C5-C9)
nasolacrimal duct opens into inferior meatus
when choanae is narrowed or blocked at birth what is this called atresia
choanae open into nasopharynx
arterial supply of inside of nose little's area aka Kiesselbach's plexus
lobes in right lung 3
lobes in left lung 2
hilar shadows on CXR made of pulmonary vessels
position of phrenic and vagus nerve phrenic passes anterior to lung root and vagus passes posterior of lung root
causes of shortness of breath (respiratory) upper airway (eg croup as a paediatric example) asthma emphysema/ pneumonia pleural problem eg pleuritic chest pain chest wall problem eg trauma respiratory/ cardiac interaction eg pulmonary embolism
causes of SOB (cardiac) cardiac failure (heart muscle problem, heart valve problem, heart rhythm problem, obstructive heart problem)
causes of SOB (apart form cardiac and respiratory) metabolic (diabetic ketoacidosis), haematological (anaemia), neuromuscular, psychological (anxiety), physiological (pregnancy), and drugs (eg aspirin or overdose)
questions to ask (HPCx) asthna when did it start when does it happen any triggers any relieving factors any associated symptoms does it restrict activity
questions to ask (PMHx) asthma signification/ previous/ongoing conditions atopic history immunisation history
explain the PEF results (variability of readings and what is considered positive) value of more than 20% variability after monitoring at least twice daily for 2 weeks is regarded as a positive result (NICE)
positive results on FeNO level of >50ppb and indicates eosinophilic airway inflammation
asthma definition chronic respiratory condition associated with airway inflammation and hyper-responsiveness
budesonide synthetic inhaled corticosteroid causing anti-inflammatory action via cellular binding and modulating gene expression
serial (anatomical) dead space volume of conducting airways (0.15l)
distributive dead space not airways and dont support gas exchange eg damaged alveoli (0.02l)
physiological dead space serial dead space + distributive dead space (0.17l)
pulmonary ventilation rate (PVR)= respiration rate x tidal volume
dead space ventilation rate = physiological dead space x respiration rate
alveolar respiration rate (AVR) = PVR - dead space ventilation rate
central chemoreceptors (CCR) found on medulla and are sensitive to changes in H+ and pCO2
peripheral chemoreceptors (PCRs) found within aortic arch and carotid arteries and are sensitive to changes in arterial pO2 and pH
permeability of BBB to substances impermeable to H+ and HCO3- but permeable to CO2 (CO2 travel into brain react with water making products detected by CCR leading to hyperventilation -> decreases PCO2)
for PCRs when does hyperventilation get stimulated when arterial pO2 falls below 13.3mmHg
increased pCO2 and response from receptors most important in CCR than PCR
fall in pH and response from receptors detected by carotid but not aortic bodies
hypoventilation leads to respiratory acidosis
hyperventilation leads to respiratory alkalosis
uncontrolled diabetes leads to metabolic acidosis
vomiting leads to metabolic alkalosis
priority of responses in ventilation PCO2 -> pH -> PO2
cheyne strokes occurs in people with CNS diseases, head trauma, intracranial pressure and heart failure where rapid breathing -> apnoea (due to delayed message relay) -> rapid breathing
respiratory depression rate/depth respiration is insufficient to maintain adequate exchange in lungs and can be reversed by analeptics eg doxapram hydrochloride
DRG (dorsal respiratory group) innervate diaphragm and external intercostal muscles having a role in inspiration- switch on for 2s and off for 3)
VRG (ventral respiratory group) innervate abdominal muscles and internal intercostal muscles for forced expiration
pneumotaxic centre in pons transmits inhibitory signals to DRG to limit inspiration and prevent over inflation of lungs
apneustic center in pons responsible for prolonged insiratory gasps (apneusis) to prolong DRG stimulation
vagus nerve sends afferent information from lungs to DRG to prevent overinflation of lungs bu switching off inspiration
cerebral cortex in ventilation bypasses medullary centers (mind over body) to an extent (will need to breath when O2 conc reaches critical levels)
hypothalamus in ventilation alters resp rate based on strong emotions, pain, temperature eg will experience apnoea when angry or tachypnoea when excited
juxtapulmonary receptors (J.C fibres) lie in alveolar wall between epithelium and endothelium (close to pulmonary capillaries) and are stimulated by congestion, oedema and histamine where activation leads to apnoea/ rapid shallow breathing, bronchoconstriction and mucus secretion
irritant receptors between epithelial cells and are sensitive to irritant gases, smoke and dust and activation results in rapid shallow breathing, cough, bronchoconstriction, mucus secretion and gasps
who should be tested for alpha-1 antitrypsin deficiency (AATD) all patients with COPD should be tested once for AATD
effect of low/ absent AATD EMPHYSEMA/COPD because theres not enough to inhibit neutrophil elastase
questions to ask when COPD suspected weight loss reduced exercise tolerance waking at night with breathlessness ankle swelling fatigue occupational hazards chest pain haemoptysis
which drug can cause ankle swelling amlodipine
Vd= dose/ To conc
formula for first order kinetic rate of elimination Ct= Coe^-kt (e= 2.718)
k= CL/ Vd
CL = K x Vd
t1/2 = 0.693/k
infusion rate = clearance x Css
F = AUC oral/ AUC IV
how many half lives does it take to reach steady state 5
dose = (for oral regimen) (CL X Css X t )/ F
dose given = amount needed / F
factors affecting design of dosage regimen (3) TW, urgency of onset of effect, and elimination half life
large TW uses what strategy maximal dose
small TW uses what strategy target level
loading dose (LD) = target level x (V/F)
maintenance dose (MD) = target level x (CL/ F)
short elimination half life <1 hour. If it has large TW then intervals of 6 or 8 but if it has small TW given by infusion +/- loading dose
moderate elimination half life 4-24 hours given initial dose, then half that every half life
long elimination half life >24 hours - set a 24 hour dosage interval to ensure best patient compliance
gentamicin antibiotic (aminoglycosides) which manages septicaemia, endocarditis and is given as IV/ IV infusion and IM in 3 divided doses or single daily dose with side effects of ototoxicity and nephrotoxicity
post antibiotic effect time needed to show regrowth following removal of antibiotic (to prevent toxicity we aim for tough <2mg/L)
gentamicin half life (t1/2) 2-3 hours in normal renal function but 30-60 hours in anephric patients
which patients should receive single daily dose of gentamicin those on cisplatin chemotherapy, those with CLcr <20mL/min, children, and those with endocarditis
single daily dose gentamicin - how much given and when give 7mg/kg in 100mL over 30-60 min and sample 6-14 hours after start of infusion
pneumonia inflammatory reaction of alveoli and interstitium caused by infection and characterised by inflammatory exudate in alveolar space that consolidates, inflammation of alveolar septa, and features of acute inflammation
how is pneumonia different to bronchitis bronchitis affects bronchi and pneumonia affects alveoli
red hepatization appearance when neutrophils and fluid in alveoli congested in capillaries
routes of infection for pneumonia aspiration, inhalation of pathogen, and contamination from systemic circulation
how can pneumonia be classified by pathogen, setting, anatomically
anatomical pneumonia classification types lobar pneumonia and bronchopneumonia
lobar pneumonia alveoli-alveoli (organism access alveoli and spread rapidly via alveolar pores to others seen in poor adults or alcoholics)
bronchopneumonia bronchi-alveoli (organisms colonise bronchi and spread to alveoli with affected areas consolidating seen in young/elderly/immobile)
community acquired: acute/typical pneumonia cause S pneumoniae (most common cause of 90% lobar- is gram positive diplococi)
causative organisms for pneumonia bacteria )gram +/-), viruses, mycoplasma, fungi, and inorganic agents (inhaled dusts or gases)
aspiration pneumonia caused by abnormal gag/swallow reflexes (from stroke/unconsciousness/repeated vomiting/ underlying disease MS) causing irritation of gastric contents and bacteria leading to often necrotising abscess formation in survivors
symptoms of acute bacterial pneumonia fever, dyspnoea, cough with purulent sputum, crackles on auscultation, consolidation in radiograph
when can pneumonia be diagnosed using what sputum (bacterial/virus is gram stained or bacterial cultured with suitable antibiotic), xray, and FBC (wbc counted)
TB is a form of what chronic pneumonia
what bacteria causes TB mycobacterium tuberculosis
symptoms of TB gradual onset anorexia, weight loss, fever (low grade remitting), night sweats, chest pain, prolonged coughing with sputum production
diagnosis of TB involves (2) sputum analysis (2- finding slender role aerobes, high content of complex lipid identified with acid fast stains, cultures to check for drug susceptibility ) and xray
pathogenesis of TB Inhale → macrophage engulfs → change pH so no phagolysosome formed -> survives in macrophage w flu symptoms/asymptomatic → lymph node cell mediated response → Th1 activation → IFN-γ → macrophage activation → granuloma → latent or active TB
types of emphysema (anatomical location) centriacinar/ centrilobar (most common in upper lobes, smoking related, dilated respiratory BRONCHIOLES) and pan acinar/ pan lobar (dilated alveoli, more common in lower lobes, is hereditary)
causes of emphysema smoking and inherited (AATD deficiency)
presentation/ symptoms of emphysema SOB and prolonged expiration, barrel chest due to use of accessory muscles, prolonged onset >40 years, congenital AATD deficiency presents earlier, often copresents with chronic bronchitis (cough + excess mucus), and pursed lips to maintain airway
bronchiectasis permanent dilation of main bronchi + bronchioles, seconfary to pulmonary inflammation and scarring causing airway to dilate as surrounding scar tissue (fibrosis) contracts
bronchiectasis symptoms chronic cough, dyspnoea, production of copious amount of FOUL SMELLING sputum, and clubbing, haemoptysis (due to damage to epithelium causes bleeding)
pathogenesis of bronchiecstasis infection (recurrent and persistent infection weakens bronchial walls), obstruction (inters with drainage of bronchial secretions), and congenital/ hereditary (CF-> infection, immunodeficiency -> infection etc)
bronchiectasis morphology lower lobes on both sides, vertical air passages, 4x expanded, affected lobes surgically removed
acute restrictive lung disease ARDS
chronic restrictive lung disease pulmonary fibrosis and pneumoconioses
type I pneumocyte squamous and extremely thin, cover 95% alveolar space, involved in gas exchange
type II pneumocyte granular and cuboidal, cover 5% alveolar space and secrete pulmonary surfactant
fibrosis Excessive formation of scar tissue due to chronic injury or inflammation (inflammation of alveolar walls attract macrophages + fibroblasts -> fibroblasts lay down collagen decrasing lung compliance)
obstructive disease overview limited airflow due to obstruction caused by increased airway resistance
restrictive disease overview restrict normal lung movement due to reduced expansion of lung tissue and decreased total lung capacity
pneumoconioses from workplace, develop over a long time even after exposure stops which increases risk of cancer
pleural effusion causes (2) exudate from cancer of pneumonia and congestive heart failure/ kidney or liver disease (transudate)
symptoms of pleural effusion SOB, chest pain on breathing in deeply, fever, cough
treatment of pleural effusion drain or treat cause with antibiotics
majority of epithelium from nasal cavity to bronchi pseudostratified columnar ciliated epithelium
lining of bronchioles simple columnar to cuboidal epithelium
lining of alveoli thin squamous epithelium
conducting segment of airway nostrils to terminal bronchiole
respiratory segment of airway respiratory bronchioles to alveoli
lining of nasal vestibule keratinised stratified squamous epithelium
oropharynx and laryngopharynx lining non keratinised stratified squamous epithelium
function of turbinate bones in nasal cavity create turbulence driving air in and out sinuses
how many lobar bronchis on the right 3
how many lobar bronchis on the left 2
histological sites in respiratory system (4) mucosa (respiratory epithelium and lamina propria), submucosa, cartilage and o muscular layer, and adventitia
lamina propria in respiratory system contains CT, blood, and lymph
cartilage in trachea c shaped hyaline cartilage
club cells found in terminal bronchioles only to repair airway after injury, secrete antiinflammatory and immunodulatory proteins etc MAKE SURFACTANT TOO
cilia features membrane bound, centriole derived projections + microtubule cytoskeleton, 9+2 ciliary axoneme, dynein arms for motility
Created by: kablooey
Popular Medical sets

 

 



Voices

Use these flashcards to help memorize information. Look at the large card and try to recall what is on the other side. Then click the card to flip it. If you knew the answer, click the green Know box. Otherwise, click the red Don't know box.

When you've placed seven or more cards in the Don't know box, click "retry" to try those cards again.

If you've accidentally put the card in the wrong box, just click on the card to take it out of the box.

You can also use your keyboard to move the cards as follows:

If you are logged in to your account, this website will remember which cards you know and don't know so that they are in the same box the next time you log in.

When you need a break, try one of the other activities listed below the flashcards like Matching, Snowman, or Hungry Bug. Although it may feel like you're playing a game, your brain is still making more connections with the information to help you out.

To see how well you know the information, try the Quiz or Test activity.

Pass complete!
"Know" box contains:
Time elapsed:
Retries:
restart all cards