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Exam Prep > Medical Conditions/Patho of > Flashcards

Medical Conditions/Patho of Flashcards

1
Q

What is angina? How does it present?

A
  • angina is chest discomfort due to myocardial ischemia (heart is not getting enough oxygen) - increase in demand, decrease in supply
  • pain occurs due to build up of CO2 and lactic acid
  • often it displays as a squeezing/heavy sensation, it may radiate, deep breathing may increase the pain
  • often resolved by decreasing the demand or increasing oxygen levels
  • can lead to infarct if not corrected
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2
Q

Stable angina

A
  • typical and predictable
  • often due to increase in workload to the heart
  • will come with heavy/squeezing sensation but is typically not long lasting (uncommon to last beyond 30 minutes)
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3
Q

Patho of Angina

A
  • due to coronary artery obstruction leading to a difference between the oxygen supply and demand
  • the demand for oxygen goes up, but the heart can not keep up leading to pain (therefore, need to provide heart with more oxygen or get it to rest)
  • commonly due to CAD (build up of plaque)
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4
Q

Unstable angina

A
  • could be sign of pre-infarct
  • often symptoms come at rest, can not be relieved with meds/oxygen, and are more severe than typical angina (often lasts more than 20mins)
  • from blood flow to the heart being slowed by narrowed vessels or small clots that formed in coronary arteries
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5
Q

Variant angina

A

“transient” or “prinzmetal”
- due to spasm of coronary artery often while sleeping
- often not long lasting but can lead to MI/lethal arrhythmias
- common in type A personalities, people who smoke, females

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6
Q

Takotusbo Cardiomyopathy

A
  • sudden onset of chest pain which mimics an MI
  • due to emotional stress and release of stress hormones
  • also known as broken heart syndrome
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7
Q

Brugada syndrome

A
  • sudden death during sleep from lethal arrythmias
  • from sodium gene mutation causing ventricles to beat irregularly, leading to blood circulation being improper
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8
Q

Myocardial Infarction

A
  • prolonged ischemia
  • presents with angina like pain (pressure, squeezing), pain may radiate, may have N/V,
  • rest/meds will not help
  • some people (especially women) may present as unwell or N/V only - no chest pain
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9
Q

Patho of Myocardial Ischemia

A
  • tissues become damaged due to lack of oxygen, often due to plaque build up
  • injured tissue will have a fibrin mesh/clot form - the tissue is injured from lack of oxygen/blood flow
  • injured tissue cells will die if ischemia is not reversed (infarct is when they die)
  • MI occurs when ischemia has lasted long enough to cause cell death due to cut off blood supply - pain is due to CO2 and lactic acid build up
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10
Q

What are acute MI’s caused by?

A

usually from a thrombus formation, or can be from hypovolemia (global ischemia)

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11
Q

What is one way in hospital that MI’s are detected?

A

troponin release
- troponin is a regulatory protein found in the heart/skeletal muscle that is released when injury has occurred to the myocardium
- higher levels lead to a greater chance the patient has had an MI

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12
Q

What needs to happen if patient is having an MI?

A

blocked vessels need to be reopened, often through use of stents, fibrinolytic, angioplasty

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13
Q

How do fibrinolytics work?

A

they work by activating plasminogen which forms plasmin
- plasmin breaks down fibrin (which is found in clots)

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14
Q

What is an angioplasty? A stent?

A

A - unblocking a vessel through the use of a balloon which will push the plaque outwards against the artery wall
S - an insertion of a tube (metal or plastic) into artery to open and keep the artery open

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15
Q

What is the aftermath of the heart in the case of an MI?

A
  • the necrotic tissue is replaced by scar tissue over the few weeks after an MI
  • the scar tissue is a poor conductor, can nor contract and decreases the hearts effectiveness - potential for arrhythmias
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16
Q

The two forms of treatment for chest pain are nitro and ASA. How does nitro work?

A
  • nitric acid is used for relaxation of smooth muscle. nitro will be converted to this in the blood
  • it will help to relax smooth muscle and vasodilate which will help lessen chest pain
  • decreases your preload (pressure at the beginning of systole)
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17
Q

How does ASA work in terms of chest pain?

A

“COX blocker” or Thromboxane A2 inhibitor
- inhibits cyclooxygenase which is needed to make thromboxane A2 (which promotes platelet aggregation and vasoconstriction)
- reduces platelet aggregation which will stop a clot from progressing

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18
Q

What is an aneurysm?

A
  • an aneurysm is when part of an artery wall weakens causing it to balloon out/widen abnormally
  • can be caused from high blood pressure on arterial walls, atherosclerotic disease, infectious disease (syphilis), genetic disorders, trauma
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19
Q

Two classifications of aneurysms?

A
  • saccular (sac-like)
  • fusiform (tube-like)
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20
Q

Abdominal aneurysm - what is it?

A
  • often not known until leaking/rupture occurs (when symptoms start)
  • usually begin as small tear in intima allowing blood to leak in aorta and the tear will eventually continue outwards causing bleeding to continue into other areas of the body
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21
Q

Signs of an abdominal aneurysm:

A
  • mass seen in stomach region (may be pulsing)
  • pain goes from abdomen to back (excruciating)
  • might become hypotensive, syncopal
  • could be bradycardic (vagus nerve stimulation due to being around the aorta)
  • might have rigidity to abdomen
  • femoral pulse may be absent
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22
Q

Thoracic aneurysm - signs?

A
  • can cause severe pain beginning in the back spreading to abdomen
  • may have difficulty swallowing, cough, wheezing, unequal pressures in the arms
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23
Q

Dissecting aneurysm - what is it?

A
  • aneurysm will start as tearing allowing blood to start to move through the layers of the wall due to increased pressure
  • as more blood moves, it will eventually rupture the outer wall leading to mass hemorrhage into the thoracic/pleural cavities
  • hypertension is a common factor contributing to an aneurysm dissecting
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24
Q

Signs of a dissecting aneurysm:

A
  • excruciating pain described often as a ripping sensation (can be in back/abdomen/epigastric region/extremities)
  • they will be sweaty/pale
  • may have pulse deficits, BP may become unattainable
  • person may be syncopal
  • may have signs of blood pooling
  • may be altered mental status (blood not getting to brain)
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25
Q

Pericardial tamponade - what is it? what can cause it?

A

Tamponade is when the pericardium (sac surrounding the heart) fills with blood leading to inadequate filling of the heart and less cardiac output
- can be caused by a AAA if it dissects to the heart, trauma, pericarditis

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26
Q

Signs of pericardial tamponade:

A
  • chest pain
  • Becks triad: JVD, muffled heart sounds, hypotension
  • tachycardia
  • resp distress
  • dizzy/faint
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27
Q

What is thrombophlebitis? What is DVT?

A
  • inflammation of vein wall
  • blood clot forming (often in legs)
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28
Q

Patho of DVT

A
  • blood clot will form blocking flow of blood in a vein
  • often occurs in legs, the issue is if it breaks off forming an embolus that can travel to the lungs
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29
Q

What factors impact chance of a DVT?

A
  • smoking
  • birth control
  • trauma
  • recent surgery
  • pregnancy
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30
Q

What is congestive heart failure? What causes it?

A
  • condition when the heart can not pump blood to meet the needs of the tissues
  • can be caused by too much volume, too much pressure, loss of myocardial tissue (can not pump properly), impaired contractility (pump does not work)
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31
Q

Left sided heart failure

A
  • left ventricle can not pump properly causing blood to back up into pulmonary circulation
  • can be due to hypertension, valve heart disease
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32
Q

What are the forward effects of left sided heart failure?

A
  • less ventricle emptying = less cardiac output
  • less perfusion of tissues
  • RAS system will activate, so more sodium/water reabsorbed = increase in BP
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33
Q

What are the backwards effects of left sided heart failure?

A
  • JVD
  • pulmonary edema
  • crackles
  • wheezing
  • pink tinged sputum
  • SOB
  • agitation/anxiety (due to hypoxia)
  • elevated heart rate
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34
Q

Right sided heart failure

A
  • often due to left sided heart failure causing too much pressure in pulmonary circulation
  • due to increase in workload on right side, pump will fail
  • can be due to hypertension, COPD, PE, right sided infarct
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35
Q

Right sided heart failure symptoms

A
  • peripheral edema in legs
  • ascites in abdomen (fluid)
  • venous congestion (will cause distention in organs like liver/spleen that are distendable)
  • increased blood volume systemically
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36
Q

How is CHF treated?

A
  • ACE inhibitors
  • angiotensin receptors blockers
  • beta blockers
  • diuretics
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37
Q

What is flash pulmonary edema?

A
  • rapid accumulation of fluid in the lungs
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38
Q

What is insulin’s role in the body?

A
  • when blood glucose rises, pancreas releases insulin
  • insulin will transport glucose into cells to be used for energy or it will take up the glucose and have it stored as glycogen in the liver for later use (will decrease blood sugar levels)
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39
Q

What is glucagon’s role in the body?

A
  • when glucose levels fall, it will increase levels through glycogenolysis or gluconeogensis
  • glyco (breakdown of glycogen to glucose in liver to be released for use by cells
  • gluco (turning to fat metabolism to get energy)
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40
Q

When blood sugar levels fall, what are common signs?

A
  • combative/aggressive/altered
  • slurred speech/ won’t make sense
  • “drunk like”
  • sweaty
  • dilation of pupils
  • tachycardia
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41
Q

What is type 1 diabetes?

A
  • beta cells in pancreas produce no insulin
  • need insulin injections and often strict diet/exercise regimen
  • diagnosed young
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42
Q

What is type 2 diabetes?

A

Non-insulin dependent
- beta cells produce insulin but not enough to meet bodies needs/cells become desensitized to it
- diagnosed later in life
- impacted often by lifestyle

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43
Q

What is HHNK?

A
  • commonly seen in type 2 diabetics (often elderly)
  • high blood sugar levels often caused by not following proper treatment plans, illness/infection, certain meds like diuretics
  • body will try to pee out excess glucose leading to chance of severe dehydration if not treated
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44
Q

Signs of HHNK

A
  • polyuria/polydipsia (excessive peeing/thirst)
  • dry mouth
  • warm, dry skin
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45
Q

What is DKA?

A

Diabetic Ketoacidosis
- type 1 diabetes: not enough insulin, can not take up glucose to use for energy
- body turns to burning fats for energy leading to production of ketones

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46
Q

Signs of DKA:

A
  • polydipsia, polyuria
  • high blood sugar
  • acetone breath, kussmauls resps
  • hypotensive
  • high heart rate
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47
Q

What are some things used to diagnose someone with diabetes?

A
  • polyuria, polydipsia
  • wounds that do not heal
  • weight loss
  • numbness in feet
  • high fatigue
  • dizzy, blurred vision
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48
Q

What are the role of beta, alpha and somatostatin cells?

A

beta - produce insulin
alpha - secrete glucagon
somato - decrease levels of insulin/glucose in blood

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49
Q

Why do seizures occur? Some common causes?

A
  • electrical activity in the brain becomes abnormal causing erratic firing of neurons
  • symptom of an underlying issue
  • common causes include: tumors, trauma, hypoglycemia, overdose/toxicology, infection, fever, epilepsy, eclampsia, stroke, brain defects/bleeds
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50
Q

Tonic clonic seizures

A

Grand mal
- sudden tonic muscle bilateral contractions, followed by clonic phase (relaxation phase)
- often have no warning, and a postictal phase will follow
- incontinence is common, oral injury is common

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51
Q

Petit Mal seizure

A

Absence
- non-convulsive, lasting 1-10 seconds
- may have automatism, repetitive activities
- often can return to normal active immediately following

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52
Q

Atonic seizure

A

Drop attack
- sudden loss of muscle tone
- cause of falls, head will droop, jaw will go slack

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53
Q

Simple partial seizures

A

Focal
- involves one hemisphere of the brain
- have an aura prior to
- may have tremors in impacted area of brain, tingling sensation, may go flush/be tachy/hypotensive but no LOC

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54
Q

Complex partial seizure

A

Temporal lobe seizures
- may have automatism, hallucinations, deja vu
- patient will have postictal phase - will not remember event
- often misdiagnosed as psych problem

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55
Q

Pseudoseizures

A
  • seizure like activity due to psych disturbance
  • movements tend to be bilateral, symmetrical
  • can sometimes be interrupted with sharp command
  • incontinence/injury rare
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56
Q

Febrile seizures

A
  • seizure due to fever often in children between 9 months-5 years
  • often occur within first 24 hours of illness
  • often stops on it’s own within a few minutes
  • child may tighten on both sides of body, cry/moan, eye rolling, vomit, pass urine, sometimes stop breathing/turn blue, not responsive to parents voice
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57
Q

What is epilepsy?

A

CNS disorder where brain activity becomes abnormal
- can be developed at birth, from trauma, infection, tumors

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58
Q

What is status epilepticus?

A
  • a seizure lasting longer than 5 mins, or having more than one seizure in short period of time without regaining consciousness
  • medical emergency that can lead to brain damage due to hypoxia
  • may have convulsions or may look like they are day-dreaming/acting irrational
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59
Q

What is a CVA?

A

Cerebrovascular Accident (Stroke)
- interruption of blood flow to the brain leading to cerebral infract/neuro deficits due to lack of oxygen/blood flow

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60
Q

What causes a stroke?

A
  • thrombus
  • embolus
  • hemorrhage in the brain
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61
Q

Ischemic Stroke

A
  • due to blocking of an artery that supplies blood to the brain (tumour, atherosclerosis)
  • slow developing but most common
  • might have history of stroke, angina, vessel disease
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62
Q

Hemorrhagic stroke

A
  • bleeding into brain tissue from burst vessel leading to ischemia, rising ICP
  • often occurs at points of exertion/stress
  • rapid deterioration
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63
Q

Intracerebral Hemorrhage (stroke)

A
  • bleeding into brain often due to hypertension
  • cerebral vessels will develop aneurysms
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64
Q

Subarachnoid hemorrhage (stroke)

A
  • caused by rupture of aneurysm
  • presents as a severe headache with nuchal rigidity and photophobia
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65
Q

What is the main treatment for strokes?

A

tPA - tissue plasminogen activator
- dissolves blood clots, but needs to be within the 6 hour window
- will turn plasminogen to plasmin (which breaks down clots)

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66
Q

What is a TIA?

A

Transient Ischemic Attack
- mini stroke
- symptoms typically resolve within an hour, but it is often a precursor to a CVA
- often from atherosclerosis

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67
Q

What are common findings in strokes?

A
  • facial droop
  • arm/leg drift
  • unilateral weakness
  • slurred speech/mute
  • have gaze to one side
  • high BP
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68
Q

What are some things that can mimic strokes?

A
  • postictal patients
  • infection
  • tumor
  • toxicology
  • trauma (bleed)
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69
Q

What is meningitis?

A

Inflammation of the meninges around the brain/spinal cord
- can be viral or bacterial

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70
Q

Symptoms of meningitis

A
  • severe headache
  • nuchal rigidity
  • fever
  • altered mental status
  • photophobia
  • rash (petechia)
  • seizures
  • N/V
  • recent infection
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71
Q

Kerning’s sign

A

when hip is flexed to 90 degrees, can not straighten leg

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72
Q

Brudzinski’s sign

A

severe neck stiffness, pts knees/hips flex when neck is flexed

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73
Q

What are the two bacteria that can cause meningitis?

A
  • streptococcus pneumonaie (pnuemococcus)
  • neisseria meningitdis (meningoccous)
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74
Q

What is anaphylaxis?

A

severe, life-threatening allergic reaction

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75
Q

What are the steps in an allergic reaction?

A
  1. initial contact with allergen will be made
  2. antibodies (IgE) will be made and will bind to mast cells and wait for another exposure
  3. re-exposure happens, the antigen will bind with the antibody causing degranulation of mast cell to release mediators (histamine)
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76
Q

What is the function of histamine in an allergic reaction?

A

purpose is to increase capillary permeability to white blood cells and proteins to allow them to engage with pathogens in tissues

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77
Q

Effects of histamine

A
  • vasodilation (patient becomes hypotensive)
  • contraction of smooth muscle (bronchoconstriction, GI troubles - N/V)
  • increase in capillary permeability (can lead to hypotension, fluid shifting, less CO)
  • swelling of the face, throat, eyes, mouth
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78
Q

Leukotrines

A
  • mediator of allergic reaction
  • bronchoconstrictor
  • causes wheezing
  • coronary vasoconstriction
  • cap permeability
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79
Q

Eosinophils

A
  • attracted to the allergic reaction
  • deactivates leukotrienes to turn off reaction
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80
Q

Neutrophils

A
  • apart of inflammatory response
  • recruit cells of the immune system
  • help kill pathogens
81
Q

What are the 5 system symptoms in anaphylaxis to look out for?

A

cardio - tachycardia, hypotensive, dizzy
resp - throat tightness, SOB, wheezing
GI - N/V, diarrhea, abdominal pain
neuro - headache, anxiety, sense of doom
skin - redness, hives, swelling

82
Q

What is late phase or biphasic anaphylaxis?

A
  • a reaction will occur, symptoms have onset but resolve
  • rebound reaction occurs without having secondary reaction
83
Q

The main drug in anaphylaxis treatment is Epinephrine - how does it work?

A

alpha 1 stimulation - will cause vasoconstriction (they are vasodilated)
beta 1 stimulation - will increase preload as beta 1 is cardiac (will increase force, contractility)
beta 2 stimulation - will cause bronchodilation (these patients are constricted)

84
Q

Dosing in epi pens

A

0.3mg - adult dose
0.15mg - child dose

85
Q

What happens if person pricks their finger with epi pen by accident?

A
  • site will go blanched (necrosis can occur)
  • need phentolamine to reverse impacts
86
Q

Granulation tissue vs. keloid scars

A

gt - new tissue which grows above capillary bed after a burn/wound to heal
k - web like scar made of granulation tissue, can interfere with body function in that area/is disfiguring

87
Q

What are 4 sources of burns?

A

thermal - flame, heat, touching hot object
chemical - substance reacts on tissue
electrical - arking (electricity jumps) or flash over (combustion up close)
radiation - UV rays

88
Q

What can lead to resistance against getting a burn?

A
  • water content in skin
  • thickness/colour of skin (hair, oils)
  • circulation of skin (ability to let off heat)
89
Q

Three zones of injury for burns

A

zone of hyperemia - has good perfusion (inflammatory response heightens the perfusion)
zone of perfusion - decreased perfusion, but can be saved. tissue area we most focus on
zone of coagulation - tissues completely dead (third degree burns)

90
Q

First degree burns

A
  • epidermis damage only
  • blanching, redness
  • heal on it’s own
  • such as a sunburn
91
Q

Second degree burns

A

Superficial or deep partial thickness burns
- with superficial often there is blisters, redness, damages epidermis to dermis
- risk of infection
- deep, goes down to basal layer of dermis
- will have diminished sensation in the area
- can be red/wet (cells leaking) or white/dry (cells destroyed)

92
Q

Third degree burns

A

Full thickness
- epidermis and dermis completely destroyed
- sensation absent, but high pain around the area
- eschar present (charring of skin)

93
Q

What is number one complication with burns?

A

infection

94
Q

Rules of nines for adults

A

Way to calculate burn %
- each arm is 9% (4.5 front and back)
- upper chest is 9%, abdomen is 9%,
- whole back = 18%
- each leg = 18%
- head = 9%
- genital area = 1%

95
Q

Rules of nines for children

A
  • head is 18% total
  • each arm is 9%
  • body is 18% on front, 18% on back
  • each leg is 14% total
  • genitals is 1%
96
Q

What is the systemic response to burns?

A
  • potential for hypovolemic shock is high
  • fluid shift will lead to leaking of capillaries
  • total volume will decrease, decreased oxygen to organs, decreased return/output
97
Q

Burns effect on the kidneys

A

Renal failure can occur due to 2 reasons:
- hemolysis: RBC breakdown
- rhabdomyolysis: muscles breakdown releasing substances (myoglobin) into bloodstream

98
Q

Burns impact on the capillaries

A
  • histamine will be released (vasodilation, increase in permeability)
  • hypotension, fluid shifting
  • sodium loss (hypernatremia)
  • blood will become more viscous due to loss of blood volume - clot risk - less perfusion to tissues/organs
  • potassium released due to cell damage (hyperkalemia)
99
Q

Overall complications of burns

A
  • infection is #1 killer
  • renal failure
  • lung damage (ARDS)
  • electrolyte imbalances
  • sluggish blood flow (clot potential)
  • decreased heart contractility (less blood flow)
100
Q

Formula for fluid therapy for burn patients

A

Parkland formula
- 4ml/kg X TBSA (% burned) - 50% given in first 8 hours, other half given within next 26 hours after that

  • don’t bolus as due to fluid shifting it will leak into extracellular space instead
101
Q

How to treat burn patients

A
  • oxygen is a must (to help CO poisoning, decrease in perfusion)
  • remove clothing (traps heat)
  • if 1st degree burns: moist, sterile dressing
  • if 2nd degree burns under 15% BSA: moist sterile dressing
  • if 2nd degree burns >=15% BSA: dry sterile dressing
  • if 3rd degree burns: cover all with dry sterile dressings
102
Q

Signs of carbon monoxide poisoning

A
  • weakness
  • dizzy
  • N/V
  • SOB
  • confusion
  • LOC
  • blurred vision
  • headache
103
Q

Why is CO poisoning with burns such a risk?

A

CO affinity for hemoglobin is 250x larger than oxygen’s
- 20% CO poisoning is when symptoms begin to show
- 60% is fatal

104
Q

Chemical burns - strong acids

A
  • the burning will cause coagulation of proteins which will act as a buffer to halt the burning process
  • denatures the proteins in the skin so they clump together
  • such as HF acid
105
Q

Chemical burns - aklakli’s

A
  • more dangerous as substances can diffuse deeper into tissues due to liquefaction necrosis of tissue
  • drain cleaners, fertilizers
106
Q

How to treat chemical burns?

A
  • flush all chemical burns
  • for eye burns, keep cool cloth over eyes and have them keep eyes closed
  • flush eyes for 15-20 mins
107
Q

Different electrical injuries/burns

A
  • direct contact: right to source, often have exit/entry wounds
  • arcing injuries: electricity jumps from something to person
  • flash burns: electrical source comes into contact with something that is combustible - does not pass through person
108
Q

What is the killing potential with electricity?

A

the voltage (force)

109
Q

Two types of currents:

A
  • alternating: can go back and forth - can get stuck
  • direct: one shot deal - person will fly from source
110
Q

How does electricity travel?

A
  • lower voltage - will take path of least resistance
  • higher voltage - will take shortest path
111
Q

Impacts of electrical injury

A
  • exit/entry wounds
  • arrythmias
  • ventilation impairment (medulla/pons impacted)
  • brain tissue injury
112
Q

3 types of solutions

A

Isotonic: solute concentration equal in and outside of cell

Hypertonic: solute concentration greater outside the cell - water will travel to where there is more (so outside)

Hypotonic: solute concentration greater inside cell (water will move into cell)

113
Q

What four things impact fluid accumulation in interstitial spaces?

A
  • capillary hydrostatic pressure
  • oncotic pressure
  • capillary permeability
  • lymphatic channels
114
Q

How does edema occur?

A
  • hydrostatic pressure in capillaries goes up, pushing fluid out
  • oncotic pressure goes down, less fluid will be pulled from outside the vessel into the cell
  • increase in permeability, so more fluid can shift out
  • lymphatic system not working: less fluid being picked up
115
Q

Local vs. Generalized edema

A

Local - in one area - can compare body parts
Generalized - will be throughout whole leg for example

116
Q

Where is edema usually present?

A

in lower legs - higher up it goes means the more severe
- may see pitting edema - can show severity
- due to underlying illness

117
Q

Signs of fluid excess

A
  • crackles
  • increase in BP
  • neuro changes
  • edema
118
Q

What are normal levels of sodium in blood?

A

135-145 mEq

119
Q

What happens when sodium levels change in the body?

A

if low - aldosterone released to hold on to salt (water by association)
if high - ADH will be secreted (water will be held on to, it will dilute salt)

120
Q

Hyponatremia

A
  • low sodium, excess of water
  • can be from things like burns, vomiting, excess intake, adrenal problems (low aldosterone)
  • can see muscle cramps, seizures, confusion
  • high risk for athletes (hydrating with water only)
121
Q

Hypernatremia

A
  • high sodium, low water
  • may present similar to hypo - not common
122
Q

What are normal potassium levels? What can happen if potassium gets thrown out of normal range?

A

3.5-5 is normal level
- vital for heart electrical activity (can lead to arrhythmias)
- vital for metabolic processes

123
Q

How does potassium impact acidosis/alkalosis?

A
  • acidosis is an increase in hydrogen, more H+ ions move into cell - potassium will move out (hyperkalemia)
  • alkalosis is decrease in hydrogen, more H+ ions move out of cell - potassium will move in (hypokalemia)
124
Q

Hypokalemia Symptoms/signs on ECG

A
  • can be hypotensive, have cardiac arrhythmias, vomiting, muscle weakness
  • lengthening PR interval, flat T waves, U wave develops
  • need potassium
125
Q

Hyperkalemia signs on ECG

A
  • more severe than hypo
  • peak T waves, wide QRS, sine wave
  • needs calcium, bicarb to treat the acidosis
126
Q

Purpose of calcium in body, how it is regulated?

A

For hormone secretion, bones, muscle contraction
- if low, PTH is released to hold on to calcium
- if high, calcitonin will be used to bring calcium from blood to bone

127
Q

Hypocalcemia

A
  • decreased intake or increased secretions
  • will have weak bones/muscles, neurological issues
  • can be from vitamin D decrease
  • need calcium
128
Q

Hypercalcemia

A

Excessive calcium in the blood
- can be from too much vitamin D, medications, metabolic causes (tumors)
- can have muscle weakness, bone pain, kidney stones, dysrhythmias
- need calcitonin

129
Q

Heat cramps

A
  • brief muscle spasms/cramps that occur due to worked muscles (legs, abdomen are common areas)
  • occurs in people who only hydrate with water (loss of electrolytes) - common in athletes
130
Q

Heat exhaustion

A
  • people working in hot environments
  • will have cool/moist skin, headache, nausea, dizziness, only slightly higher body temp or normal
131
Q

Heat Stroke

A
  • can be fatal
  • complete failure of regulatory mechanisms
  • high body temp, will not be sweating, red/hot skin, altered LOC, shallow breathing, resps deep or shallow, rapid pulse
  • can be from heat waves or exertiom
  • heat sensitive cells of CNS can be damaged leading to brain damage
  • alcoholics, very young or old most impacted
132
Q

Hypothermia

A
  • starting around 35 degrees, it is a decrease in core body temp
  • due from heat loss or decline in heat production
  • may have shivering, numbness, slow pulse, altered LOA, lethargic, decreased BP
133
Q

How to manage hypothermia patients?

A
  • remove wet clothes
  • passive rewarming
134
Q

Frost bite

A
  • freezing of soft tissue
  • can be superficial or deep (underlying tissues)
  • will have lack of feeling to area, skin may be waxy, cold to touch, can have discolouration
  • ice crystals will form in ECF, water is drawn out of cells initially and cell membrane is damaged
  • electrolyte imbalances can occur
  • local edema leading to loss of blood flow and ischemia
135
Q

What is COPD?

A
  • emphysema and bronchitis are the two main forms
  • causes SOB
  • have chronic resp acidosis due to air trapping (increase in CO2) - they compensate by producing more bicarb
136
Q

What is emphysema?

A
  • loss of lung elasticity due to protease enzyme, destruction of alveolar walls
  • enlargement/weakening of air spaces
  • airways can collapse upon expiration trapping air
137
Q

What is bronchitis?

A
  • enlargement of submucosal glands
  • more goblet cells = more mucus
  • mucus plugging occurs causing airway obstruction and inflammation of tissues
138
Q

Symptoms of emphysema

A
  • pursed lip breathing
  • dyspnea
  • barel chested
  • accessory muscle use
  • often thin presentation
  • tripod positioning
139
Q

Symptoms of bronchitis

A
  • cough/sputum
  • can be cyanotic in colour
  • clubbing
  • increase in resp rate
  • crackles
  • perpheral edema
140
Q

Polycythemia

A
  • disorder where bone marrow produces too much RBC from hormone erythropoietin
  • an increase in blood cells = thicker blood
  • leads to right ventricular hypertrophy as blood is more viscous, harder to move
141
Q

Cystic Fibrosis

A
  • genetic disorder that impacts lungs due to mutation in CFTR gene
  • abnormal sodium/chloride transport leading to thick secretions
  • SOB is most serious condition due to mucus build up, stagnant mucus also leads to infection
142
Q

What is pneumonia?

A
  • inflammation of lungs which usually occurs for bacterial reasons but can be from viral causes or aspiration
143
Q

What is typical pneumonia?

A
  • infection from bacteria
  • causes inflammation and fluid to go into air spaces
  • usually lobar (to one lobe/area)
144
Q

What is atypical pneumonia?

A
  • from viruses
  • less striking findings impacting the alveoli septum and the lung support tissues
145
Q

Community vs. hospital acquired pneumonia

A

Community - infections due to community, diagnosed within 48 hours of hospital admission (not a resident of health facility in previous 14 days)
Hospital - starts 48 hours after admission, common cause of hospital infection

146
Q

Aspiration pneumonia

A

Aspiration of gastric juice
- symptoms often delayed so high fatality rate
- common in people with dysphagia (stroke patients, spinal injuries, trach)

147
Q

Symptoms of pneumonia

A
  • cough with sputum
  • fever
  • increase in resp rate, HR
  • chest pain
  • crackles
  • sick for a few days
148
Q

Pleurisy

A
  • inflammation of pleura (cavity around lungs)
  • commonly caused by infection
149
Q

Symptoms of pleurisy

A
  • sharp chest pain worse on inspiration, sneezing, coughing (can radiate to shoulders/back)
  • may hear rubbing, scratchy sound - layers rubbing together when breathing (pleural rub)
  • SOB, fever, cough
150
Q

Pleural Effusion

A
  • fluid collection in pleural cavity that is abnormal
  • things like CHF, renal failure can cause
151
Q

Pulmonary Fibrosis

A
  • scarring/thickening of lung tissue (excess fibrous tissue)
  • idiopathic: thought to be due to repeated lung injury
  • dyspnea is main issues, chest pain can be present, crackles, not productive cough
152
Q

What is a pulmonary embolusm?

A

Blood clot in the lungs
- often starts as thrombus and then breaks off and travels to lungs

153
Q

Factors contributing to PE

A
  • trauma
  • bed rest
  • travel
  • recent surgery
  • birth control
  • smoking
154
Q

Signs of a PE

A
  • sharp often localized chest pain
  • increased WOB
  • clear lung sounds
  • chest pain - increase in HR
  • sweaty, clammy
  • leg pain/swelling
155
Q

What is a mast cell?

A

Cell part of the inflammatory reaction
- mediated by IgE
- mast cell covered in IgE antibodies - when antigen binds, it degranulates the cell releasing histamin
- aids in wound healing

156
Q

Patho of asthma

A

There is COX 1 and 2 - #1 is involved in making prostaglandins, #2 is involved with synthesis of mediators/bronchoconstriction
- hypothesis that COX1 is inhibited when asthmatics take ASA so COX2 is activated producing mediators
- due to inability to break down acid in ASA (COX is apart of this breakdown)

157
Q

Symptoms of asthma

A
  • SOB
  • accessory muscle use
  • nasal flaring
  • wheezing
  • chest tightness
  • anxiety
  • sweaty
  • can lead to exacerbation where pt would have silent chest, could be obtunded, inaudible breath sounds
158
Q

Status asthmatics

A
  • due to inflammation of airways and mucus plugging
  • causes bronchospasm
  • not reactive to regular treatment (Ventolin)
159
Q

Epidural bleed

A

between dura mater and skull
- often dictated by periods of LOC, headache
- due to temporal lobe area being hit - causing middle meningeal artery damage

160
Q

What is shock?

A

cardiovascular system collapse leading to less perfusion

161
Q

Cardiogenic shock

A

heart can not circulate properly

162
Q

Obstructive Shock

A

blood flow in heart is blocked = less output

163
Q

Hypovolemic shock

A

lack of circulating blood volume (dehydration, bleeding)

164
Q

3 kinds of distributive shock

A
  • septic
  • neurogenic
  • anaphylactic
165
Q

Neurogenic shock

A

From spinal cord injury, causing loss of tone below site of injury - may see blood pooling - loss of stimulation to vessels causing relaxation and hypotension
- bradycardia can occur due to vagal activity
- can cause organ disfunction and failure
- from CNS injury - can be from brain injury or cervical injury as well

166
Q

Septic shock

A

from infection - leads to fluid shifting/vasodilation

167
Q

What is a pneumothorax?

A

Air in the pleural space
- can be from tear in lung parenchyma
- can be spontaneous
- can be from trauma

168
Q

Athrosclerosis

A
  • fatty deposits on tunica intima which become larger often starting in childhood
  • calcium will infiltrate the area causing it to harden and become a plaque which will lead to decreased elasticity, narrowing of arterial walls
  • potential for complete occlusion of artery
169
Q

Arteriosclerosis

A
  • arterial walls become thickened
  • inability of walls to change lumen size which is made worse by hypertension
  • smooth muscle/collagen will migrate to tunica
170
Q

Chronic hypertension & the effects

A
  • heart has to work harder leading to muscle hypertrophy and eventually left ventricular failure
  • increases rates that arteriosclerosis develops, risks for CVA and aneurysm
  • increases peripheral vascular resistance/cardiac output which is why heart has to work harder
171
Q

Meds for hypertension

A
  • diuretics
  • beta blockers
  • ACE inhibitors
  • angiotensin receptors blockers
  • calcium channel blockers
  • alpha 2 agonists
172
Q

TCA overdose symptoms

A
  • wide QRS
  • blurred vision
  • bradycardia
  • dry mouth
  • urinary retention
  • acidosis
  • resp depression
  • hypotension
  • seizures
173
Q

ASA overdose symptoms

A
  • hypokalemia
  • hyperthermia
  • peripheral edema
  • altered LOA
  • resp/renal failure
  • resp alkalosis (at first) than progresses to acidosis
  • metabolic acidosis seen
174
Q

Tylenol overdose symptoms

A
  • sweating, N/V, abdominal pain, diarrhea
  • progresses to RUQ pain, liver damage
  • finally will have abdominal distention, pain and liver necrosis
175
Q

Bodies response to cold

A
  • cold receptors in skin will receive input on decreased temp and will send info to hypothalamus
  • sympathetic nervous system will be activated - NE released to constrict blood vessels, brown fat is oxidized to conduct thermogenesis, piloerection occurs, EPI released to also cause thermogenesis
  • hypothalamus activation leads to motor centers in brainstem to activate leading to contraction of skeletal muscle
  • will trigger behaviours like huddling, rubbing hands
176
Q

Bodies response to heat

A
  • receptors detect change and send info to hypothalamus
  • hypothalamus inhibits adrenergic activity of sympathetic system (inhibits vasoconstriction leading to dilation to lead to more heat loss)
  • cholinergic fibers will release Ach and stimulate sweat (most effective way to cool)
  • may have behavioural responses like lying down limbs spread out
177
Q

Heat syncope

A
  • due to heat stress, vasodilation and dehydration
  • may have electrolyte loss, blood pooling
  • changes in mental status, headache, syncopal episode, sweaty/pale skin, cool skin, rapid pulse, increased resp rate, hypotensive
178
Q

Factors contributing to frost bite

A
  • lack of protection
  • decreased circulation to extremities (smokers, tight clothing, diseases)
  • increased vasodilation (alcoholics), fatigue, dehydration
179
Q

Superficial frostbite

A
  • altered sensations: numbness, burning
  • white, waxy skin that is firm upon touch
  • once thawing occurs, injured area can be mottled, pain increases, edema, blistering, eschar can form as blisters resolve - as this peels away, red shiny skin will show
180
Q

Deep frostbite

A
  • can include muscle, tendon, bone
  • skin is white - mottled, hard to touch
  • tissue damage occurs during rewarming, tissue will become purple/black and high pain ensues and rewarmed area will remain cold, cyanotic and form eschar
  • edema can develop
  • can take weeks to determine viable tissue
181
Q

Patho behind hypothermia

A
  • body will attempt to conserve heat by causing vasoconstriction, increasing your sympathetic activity (increase hr, bp, resps)
  • body will start to generate heat by shivering - will continue till glucose stores are depleted/insulin can not uptake or temp drops below 30 - if insulin is depleted it may turn to ketoacidosis
  • thinking can become sluggish
  • extra fluid in core from vasoconstriction stimulates volume receptors to assume an increased blood volume so kidneys will cause diuresis
  • cooling can lead to fluid shift from vascular spaces leading to increased blood viscosity/less circulation
  • pathways in liver are slowed, once shivering stops cooling will increase rapidly and vitals will decline - patient will have altered LOA, be acidotic
182
Q

ECG changes for hypothermia

A
  • PR prolongs
  • QRS prolongs
  • P wave absent or abnormal
  • osborne wave develops (looks like 2 lumps)
  • high potential for v fib
183
Q

What can trigger v-fib in hypothermic patients?

A
  • aggressive suctioning
  • rough handling
  • rapid warming
  • insertion of airways
184
Q

Mild-moderate hypothermia

A
  • not lower than 32.2
  • between 32-35
  • shivering is happening, lethargy but conscious, pale/cold skin, acetone breath may be present
  • can mimic stroke in elderly
185
Q

Severe hypothermia

A
  • lower than 32 degrees
  • brain may survive for 10 mins without perfusion, low temps can lead to higher changes of survival
  • pulse may be extremely weak/almost undetectable, resps shallow, pupils non-reactive often
186
Q

Rewarming shock

A
  • afterdrop phenomenon
  • may lead to peripheral vasodilation which results in cool blood and acids returning to core
  • could cause afterdrop temp being worse than before
  • can lead to further hypotension especially with volume depletion (diuresis)
  • cool acidotic blood going back to heart = lethal
187
Q

Treatment for severe hypothermia

A
  • wrap body in blanket/foil
  • avoid suctioning vigoursly or airway manipulation
  • only do external rewarming (hot packs) for moderate hypothermia
188
Q

Patho for pulmonary embolism

A
  • thrombus breaks off and turns to embolus, which travels to lungs obstructing pulmonary circulation
  • vasoconstriction will occur leading to pulmonary hypertension
  • absent blood flow to lung causes V/Q mismatch and decrease in surfactant - shunting will occur
  • this can result in atelectasis and worsen hypoxia
  • if clot large enough, can lead to lung infarct, decreased output, shock, death
189
Q

Patho of drowning

A
  • vital tissues become hypoxic and acidotic (not blowing off CO2) which can lead to cardiac arrhythmias
  • aspirated fluid can lead to surfactant washout, increased capillary permeability, decreased lung compliance
  • cerebral hypoxia is main cause of death (within 4-6 mins)
190
Q

What is the foramen ovale?

A

hole in fetus heart between left and right atrium

191
Q

What is the ductus arteriosus?

A

vessel connecting aorta to pulmonary artery

192
Q

How does prenatal circulation work?

A
  • oxygen rick blood is given to fetus from mother via the placenta to the fetus IVC. oxygen poor blood from babies body also travels to IVC where it goes to right atrium
  • most of the blood goes from right atrium through ovale to left atrium and ventricle then pumped through aorta to babies body
  • remaining blood from right atrium goes to right ventricle, to pulmonary artery through the arteriosus and into aorta - being pumped to babies body
193
Q

RUQ organs

A
  • liver
  • gall bladder
  • right kidney
  • colon
  • small intestine
  • small portion of pancreas
194
Q

RLQ organs

A
  • colon
  • small intestine
  • appendix
  • reproductive organs (female)
  • right ureter
195
Q

LUQ organs

A
  • spleen
  • left kidney
  • stomach
  • most of the pancreas
  • part of small intestine
196
Q

LLQ organs

A
  • left ureter
  • reproductive organs
  • colon
  • parts of small intestine
197
Q

Dementia

A
  • progressive disorder resulting from diseases such as Alzheimer’s or strike
  • Alzheimer’s is main cause, can also be from forms like Lewy bodies (abnormal proteins in nerve cells)
  • often they are forgetful, can not remember things/make new memories, trouble with communicating, behaviour changes, can not recognize loved ones
198
Q

Alzheimer’s

A

A progressive disease that destroys memory and other important mental functions
- loss of neurons and the connections
- may have shrinking brain, vascular damage, free radical production
- causes dementia (underlying issue)

Exam Prep (10 decks)

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