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NURS 709 Pathophysiology > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

What stage is Syphillis most likely to infect?

A

The primary stage

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2
Q

What is the makeup of the HIV retrovirus?

A

HIV is a spherical retrovirus with a core of RNA surrounded by a lipid membrane envelope

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3
Q

What is the main target of HIV?

A

CD4 Cells

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4
Q

HIV mutates?

A

frequently with replication

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5
Q

How is HPV spread?

A

Direct contact with virus on muscousal surfaces, usually during penetration

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6
Q

How many subtypes of HPV are there?

A

Over 100, but most infections remain subclinical

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7
Q

What are two of the manifestation outcomes from different subtypes of HPV?

A

Genital warts

Cervical dysplasia and cancer

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8
Q

What is the morphology of HPV warts?

A

They may be flat or raised, but not inherently painful

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9
Q

What are the options for HPV wart removal?

A

Topical, chemical and surgical treatment options for wart removal

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10
Q

What are the current approved vaccines for HPV?

A

Gardasil
Gardasil-9
Cervarix

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11
Q

At what age are the HPV vaccines recommended?

A

ages 11-12, but can start as early as 9

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12
Q

How many doses are considered fully vaccinated against HPV?

A

2 or 3 doses depending on age at first shot

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13
Q

What percentage of HPV related cancers do the vaccines prevent?

A

> 90%

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14
Q

HPV _____________ ______________ are the most likely to spread.

A

Active legions

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15
Q

How is the herpes simplex virus spread, and where does it end up?

A

Direct contact with the virus on any mucosal surface and the virus settles in neurons

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16
Q

What are the two types of the Herpes Simplex Virus?

A

HSV-1: Usually oral ulcers
HSV-2: Usually genital uclers

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17
Q

Between Herpes initial infections and manifestations, what normally occurs?

A

An incubation period

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18
Q

What are herpes lesions like?

A

Fluid-filled, very painful and burning

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19
Q

How do antivirals help the herpes virus?

A

Herpes is known for periodic ‘flare ups’, the antiviral medication helps reduce these flairups and transmission

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20
Q

_______________ and _______________ are both bacterial infections transmitted by sexual fluids.

A

Gonorrhea and Chlamydia

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21
Q

Where are the most common entry portals for Gonorrhea and Chlamydia?

A

The Genitourinary Tract
Oropharynx
Anus

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22
Q

What are the initial symptoms of Gonorrhea and Chlamydia?

A

Most of the initial symptoms are localized to the infected area but chlamydia may have few initial signs/symptoms

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23
Q

What are the complications of untreated infections of Gonorrhea and Chalmydia?

A

Untreated infections can cause systemic problems and infertility

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24
Q

What occurs after a diagnosis of gonorrhea and chlamydia?

A

All Previous partners must be contacted and tested, and results are reported to DHEC

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25
Q

What is the etiology of Syphilis?

A

Infections with treponema pallidum, a spirochete bacteria

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26
Q

How is syphilis spread?

A

spread through contact with an infected lesion called a chancre

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27
Q

How is syphillis tested for?

A

Blood tests called T Pa antibody tests
RPR/VRDL titers

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28
Q

What are the 3 stages of syphilis?

A

Primary
Secondary
Tertiary

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29
Q

What occurs during the primary stagte of syphilis?

A

The primary stage lasts around 3 weeks to 3 months and chancre development occurs

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30
Q

What occurs during the secondary stage of syphilis?

A

The secondary stage lasts around 1 week-6 months
Rash, fever and other systemic signs and symptoms develop here

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31
Q

What occurs during the third stage of syphilis?

A

The tertiary phase occurs after years of untreated infection and can cause cardiovascular and neurological problems

Can see problems 5, 10, 15 years later

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32
Q

What are some of the characteristics of syphilis chancers?

A

They are painless, and may be not noticed if they are not present in a visible area

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33
Q

What is the treatment for syphillis?

A

Long acting penicillin

Doxycyline if a person has a PCN allergy

-because syphilis lasts in the body for so long, we don’t need high levels of pencillin we just need longevity

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34
Q

Once a treatment for syphilis has been completed, what will happen if they take an antibody test?

A

They will always continue to test positive

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35
Q

What are the steps in the HIV lifecycle?

A

Fusion/entry
Reverse Transcription
Integration
Protein arrangement/viral assembly
Virus budding and release

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36
Q

How is HIV infection spread?

A

Infection only occurs through blood, bodily fluids (semen and vaginal fluid) or perinatal transmission

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37
Q

What are the different types of blood exposures for HIV infection?

A

Accidental
Needlesharing
Accidental needle sticks
Blood transfusions

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38
Q

What are the different types of body fluid exposures for HIV infection?

A

Vaginal and anal intercourse
Oral sex is less risky

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39
Q

What is perinatal transmission of HIV?

A

HIV transmission from a pregnant person to a fetus

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40
Q

Sexual _____________ not ______________ place people at risk for HIV.

A

Sexual practices not preferences place people at risk for HIV

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41
Q

What are the prevention practices for HIV?

A

Avoid IV drug use/resusing needles
Prevention of accidental needle sticks
Blood donations screened
Universal precautions when exposure to bodily fluids
Use of condoms/barrier methods during sex
Limiting partners and testing
Testing and Treatment of pregnant indivuals

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42
Q

What is PrEP?

A

Pre-exposure prophylaxis

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43
Q

What is PEP?

A

Post-exposure prophylaxis

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44
Q

What are the CD4 counts for HIV?

A

Normal: 800-1050/mm3
Symptoms may begin around 500/mm3
Opportunistic infections begin around: 200/mm3 (Important dividing line for overall state of their immune system)

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45
Q

What are the viral load counts for HIV?

A

As immune system fails, levels may reach 10^5-10^7/mL

The goal for patients on treatment is:
On antiretrovirals, goal is to reach undetectable which is less than 20 copies in that blood sample

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46
Q

What are the primary/acute infection signs of HIV?

A

Fever
Pharyngitis
Headache
Myalgia
Weight loss
Rash
N/V/D

The skinny man with a fever, a sore throat, and a headache has sore muscles, a rash, and GI issues.

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47
Q

What is the latency phase of HIV?

A

Average asymptomatic period of 8-10 years when untreated

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48
Q

When do symptoms begin for HIV?

A

Symptoms develop when CD4 count drops below 500-350 and manifestions include:

Generalized lymphadenopathy
Neurological Diseases
Increased infections

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49
Q

What are some of the opportunistic infections of HIV/AIDS?
Viral:
Fungal:
Protozoal:
Other:

A

Viral: Herpes simplex, cytomegalovirus, EBV
Fungal: Histoplasmosis, Candida, Pneumocystis jiroveci pneumonia
Protozoal: toxoplasmosis
Other: Kapsoi’s sarcoma and other STIs

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50
Q

HIV infected CD4 cells are eventually?

A

Destroyed

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51
Q

Glycoprotein Antigens on the virus surface important for testing in what way?

A

To test for the presence of the virus in the body

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52
Q

Upon fusion of the HIV virus to the host cell which is the __________ cell, the RNA of the virus enters.

A

CD4 cell

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53
Q

The viral genetic material of the HIV virus is?

A

RNA that is then converted through reverse transcription to DNA, and the genetic material of the virus is in the same ‘language’ as the genome of the CD4 cell and is integrated into the DNA of the host cell.

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54
Q

Once the HIV viral DNA has inserted itself into the host cell, the CD4 cell?

A

Cranks out more copies of the HIV virus

Essentially, the CD4 cell is functioning as a HIV factory.

Virus buds off the CD4 cell and is off to hijack another cell

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55
Q

HIV transmission through oral sex is less risky, it can be higher risk when?

A

The person performing oral sex has breaks or sores in their oral mucosa that is higher risk

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56
Q

Which partner has a higher risk of contracting HIV during vaginal or anal sex?

A

Being the receptive partner (partner receiving bodily fluids

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57
Q

The viral load of HIV increasing then causes?

A

The CD4 cells to drop off.
Those first changes in the increase of the viral load comes before that CD4 dropoff

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58
Q

When the CD4 cell count reaches below 200/mm3 or have particular opportunistic infections, their diagnosis is then classified as?

A

AIDS

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59
Q

__________________ _________________ worsen as CD4+ counts decrease.

A

Secondary infections

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60
Q

What is the most common opportunistic infections that is considered an AIDS defining illness?

A

Pneumocystis Jiroveci pneumonia

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61
Q

What are the symptoms of Pneumocystis Jiroveci pneumonia?

A

Occurs when CD4 count is <200

Progressive and slow and usually subacute symptoms like dyspnea on exertion, cough, fever, chest pain

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62
Q

What is the prevention and treatment of Pneumocystis Jiroveci pneumonia?

A

Bactrium Antibiotics once per day if at risk

Higher doses of bactrium for active infections

Can be fatal without treatment

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63
Q

Antibiotics in an immunosupressed patient, such as a AIDS patient can lead to?

A

Candidiasis, may develop as ‘thrush’ in the mouth, in the esophagus, or rarely, in the respiratory tract

Candidiasis is considered an AIDS defining illness

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64
Q

_________ is a common virus that is only problematic when immune system is supressed.

A

CMV

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65
Q

How is CMV spread and what are the symptoms?

A

CMV is spread by body fluids

Symptoms are
blurred vision
possible blindness (retinitis)*****
Painful swallowing
Diarrhea
Neuropathies

Dr. Custer stated that if she has a patient and suspects this she immediately sends them for an eye exam because it can lead to blindness

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66
Q

CMV in the __________ is considered an AIDS defining illness.

A

Eyes

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67
Q

What are the 2 different types of HIV tests?

A

Antibody testing
Antigen/antibody tests

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68
Q

Antigen/antibody tests are available in?

A

Both at home test kits and laboratory tests

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69
Q

What is the “window period” in regards to viral testing?

A

Since antibody tests are slightly less senstitive and have a delay from the time of infection to the test being positive and this is called the ‘window period’

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70
Q

What are the basal ganglia?

A

Groups of neurons and structures in the brain

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71
Q

What are the different subsections of the basal ganglia?

A

Caudate Nucleus
Putamen
Globus
Globus Pallidus
Substantia nigra
Subthalamic nucleus

Can Peter Gladly Go Straight?

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72
Q

Where are all the basal ganglia structures located?

A

Around the thalmus

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73
Q

What is a progressive disorder of dopamine production in the basal ganglia?

A

Parkinson’s Disease

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74
Q

What specific area of the basal ganglia is affected by Parkinson’s?

A

Substantia nigra

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75
Q

What two neurotransmitters are involved in Parkinson’s disease?

A

The balance of dopamine and acetylcholine is affected. The lack of dopamine affects the purposeful movement

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76
Q

What are the manifestations of Parkinson’s disease?

A

Ridgity
Tremor (esp. at rest)
Akinesia/bradykinesia
Loss of postural reflexes
Shuffling Gait
Mask-like face

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77
Q

While Parkinson’s increases with age, what percent of the population will be diagnosed?

A

1% of the population

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78
Q

The high levels of _____________ in Parkinson’s can cause an increase in _____________ __________/___________.

A

The high levels of acetylcholine cause an increase in muscle movements/tremors

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79
Q

When in muscle ridgity worse in Parkinson’s disease?

A

At the beginning of a movement

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80
Q

What is an autoimmune disorder that targets the CNS, and is possibly initiated by a viral infection?

A

Multiple Sclerosis

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81
Q

What is the pathophysiology behind multiple sclerosis?

A

Areas of myelin in the CNS are destroyed and replaced by scar tissue and inflammation

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82
Q

What is the basic function of myelin?

A

To speed impulses down the axon

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83
Q

When is the average onset of multiple sclerosis, and what demographic is most likely to be affected?

A

Average onset is age 30 and women are more likely to be diagnosed

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84
Q

After the myelin is broken down, what is left (in concern to multiple sclerosis)?

A

Result is that hard scar tissue plaques are around nerves. This results in the signals becoming ‘broken up’ and the communication between the neurons is unclear, motor and sensory function decreases

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85
Q

What is the general pattern of multiple sclerosis?

A

Pattern is usually repeated attacked with remissions in between, but overall symptoms gradually worsen with more permanent loss of function after each attack

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86
Q

The location of lesions for Multiple sclerosis can?

A

Allow a neurologist to pinpint on brain MS is by the symptoms exhibited

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87
Q

What is the goal of treatment of multiple sclerosis?

A

The goal of treatment is to delay symptoms and degeneration not to treat

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88
Q

What are the sensory manifestations of MS?

A

Visual problems
Numbness
Prickling (Parasthesias)

These are the earliest symptoms and the most likely for a patient to notice

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89
Q

What are the motor manifestations of MS?

A

Spasticity
Weakness
Paralysis
Speech Difficulty

These only occur if the motor cortex is affected

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90
Q

What are the cerebellar manifestations of MS?

A

Vertigo
Poor Balance

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91
Q

How can MS affect the bladder?

A

If the part of the brain that control the sphincters is effected, then incontinence can occur

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92
Q

What can be mood disorders can can manifest from MS?

A

Depression-it’s unclear as to whether depression is caused by a pathophysiological standpoint, or because of the associate manifestations of MS and their effect on a persons mood

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93
Q

The Vertebral column is unable to withstand?

A

too much rotation, extention, or flexion

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94
Q

What is often effected when vertebral damage has occured?

A

The spinal cord is damaged

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95
Q

Spinal cord injuries often occur between?

A

Injuries often occur between “segments” of the spine such as between the cervical, thoracic, lumbar and sacral

Ex: C7, L1

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96
Q

___________________ ________________ may cause compression of the spinal cord and disruption of blood supply.

A

Mechanical Injury may cause compression of the spinal cord and disruption of blood supply

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97
Q

What is an acute spinal cord injury?

A

Any traumatic injury that bruises, partially tears, or completely tears the spinal cord

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98
Q

What are the common causes of acute spinal cord injuries?

A

Motor Vehicle Accidents****
Falls
Sports injuries
Metastatic diseases causing gradual damage
Osteoporosis

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99
Q

What are the two subcategories of acute spinal cord injuries?

A

Primary and Secondary

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100
Q

What is a primary acute SCI?

A

A primary acute SCI occurs at the time of injury, direct damage to the spinal cord and is permanent

(Physical injury at the moment)

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101
Q

What is a secondary acute SCI?

A

A secondary acute SCI is continued damage due to inflammation, hypoxia

(These are the things we can try to limit using mechanical/pharmological interventions)

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102
Q

Acute SCI’s cause both?

A

Motor and autonomic motor system dysfunction

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103
Q

A __________________ ____________________ in an acute SCI causes complete loss of all functions below the injury.

A

Complete Transection

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104
Q

What is considered a complete acute SCI?

A

Total loss of movement and sensation below the level of injury

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105
Q

What is considered an incomplete SCI?

A

Partial movement and/or sensation below level of injury

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106
Q

The __________ the level of spinal cord equals?

A

The higher the level of spinal cord injury the more of the body is affected

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107
Q

A C4-C6 injury will result in?

A

Tetraplegia

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108
Q

A T6 injury will result in?

A

Paraplegia from the diaphram down

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109
Q

A L1-5 injury will result in?

A

Paraplegia-full upper extremity and trunk use, progressive lower extremity use

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110
Q

A C1 injury is?

A

Often fatal because of the phrenic nerve that exits the spinal cord and control diaphram and breathing

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111
Q

A C2-3 spinal cord injury will result in?

A

Some neck control but may require a ventilator

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112
Q

What are the most common causes of thoracic-lumbar-sacral injuries?

A

Often are compression fractures

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113
Q

An S1-5 spinal cord injury will result in?

A

Patient may have foot control, but may have bladder/bowel incontinence

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114
Q

The main problem occuring from spinal nerve injuries is?

A

The loss of the normal balance between the sympathetic and parasympathetic nervous systems.

The connection between spinal ANS nerves and brain is lost below the level of spinal cord injury

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115
Q

Why are SCIs at or above T6 especially problematic?

A

Spinal shock
Excessive Vasovagal response/neurogenic shock
Autonomic dysreflexia

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116
Q

What is spinal shock?

A

Flaccid paralysis with loss of tendon reflexes/sensation below the level of injury.
Loss of bowel/bladder function
May result in widespread vasodilation

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117
Q

Spinal shock effects are greater the ___________ the level of injury, and exist on what type of timeline?

A

Spinal shock effects are greater the higher the level of injury, and exist on a variable timeline

(Normally a few minutes-brief reaction to massive impact on spinal cord)

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118
Q

Why can spinal shock result in widespread vasodilation?

A

Because the sympathetic nervous system controls vasoconstriction->the loss of connection with the sympathetic nervous system results in this widespread vasodilation

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119
Q

What is Neurogenic Shock?

A

A vasovagal response that results from loss of the sympathetic tone below the level of SCI and results in widespread vasodilation, hypotension and bradycardia**

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120
Q

What is the only situation where vasodilation and bradycardia are both present as a result from the same pathophysiology?

A

Neurogenic shock

A low BP + a low HR=neurogenic shock

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121
Q

What type of shock is neurogenic shock?

A

A form of distributive shock because the body is not low on blood volume, but the blood is not being distributed in the correct way

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122
Q

Autonomic Dysreflexia (also known as hyperreflexia) is?

A

An acute complication following high level SCIs (T6 or above) that can only occur after spinal shock and neurogenic shock have resolved

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123
Q

How long can a patient be at risk for Autonomic Dysreflexia after spinal shock and neurogenic shock have resolved?

A

A patient can remain at risk for 6 months to a year

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124
Q

What are the symptoms of Autonomic Dysreflexia?

A

Patient has severe headache/flushed skin
Bradycardia
Vasoconstriction below SCI
Vasodilation & Sweating above SCI
Overall extreme hypertension

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125
Q

Why are we seeing both vasoconstriction and vasodilation in Autonomic Dysreflexia?

A

The sympathetic response is able to do whatever it wants below the level of injury

The parasympathetic nervous system tries to compensate above the level of injury with the vasodilation

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126
Q

What can cause autonomic dysreflexia to occur?

A

Some sort of stimulus, such as
Repeat catheterization
Bowel impaction
Tight/compression socks
Pressure ulcers

-Physiological stimuli trigger the strong sympathetic response

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127
Q

What are some of the other effects of SCI?

A

Loss of temperature regulation
Risk of DVTs and edema
Skin Breakdown
Neurogenic bladder and recurrent UTIs

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128
Q

What are the manifestations of diffuse brain injuries?

A

Altered LOC and behavior changes
-Confusion
-Lethargy
-Obtundation (less and less responsivness)
-Stupor
-Coma
-Reduced GCS score
-Decorticate/Decerebrate posturing
-Respiratory changes
-Loss of pupillary reflexes

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129
Q

How is does our brain coordinate consciousness?

A

Consciousness is coordinated by cerebral hemispheres and reticular activating systems

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130
Q

What are the ratings of the Glasgow Coma Scale?

A

Eye opening (1-4)
Motor response (1-6)
Verbal response (1-5)

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131
Q

A lower number on the GCS means?
What is a normal functioning score?

A

The lower the number, the worse the patient
“Below 8, intubate”

A normal functioning score is a 15

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132
Q

At what GCS score do we start to say “Patient is in a coma”

A

3-5

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133
Q

What is decorticate posturing?

A

Flexion of the arms and hands to the chest

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134
Q

What is Decerebrate posturing?

A

Extension of arms and hands to one’s side

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135
Q

Both Decorticate and Decerebrate posturin indicates?

A

Significant brain damage due to brainstem problems

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136
Q

Respiratory changes indicating diffuse brain injuries are?

A

Tital volume is shallow
Rate, depth, regularity

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137
Q

What manifestation of diffuse brain injuries is seen in the eyes?

A

The pupillary reflexes are no longer able to constrict or have mismatched constriction

In very severe cases, the pupils stay fixed and dilated

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138
Q

What are some of the mechanisms of brain injuries?

A

Hypoxia
Ischemia
Excitatory Amino Acid Injuries
Cerebral Edema (Vasogenic/cytotoxic)

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139
Q

What occurs during a hypoxic brain injury?

A

The brain is deprived on oxygen even though it still maintains good perfusion

Ex: Patient is in respiratory failure

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140
Q

What occurs during an ischemic brain injury?

A

Reduced blood flow to brain (can be localized, like in a stroke) or generalized

Both O2 and glucose missing (Neurons cannot get nutrition from anything but glucose)

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141
Q

What amino acid is responsible for excitatory amino acid brain injuries?

A

Glutamate

142
Q

In a vasogenic cerebral edema what occurs?

A

Fluid leaks from the intracellular fluid in to the interstital fluid

143
Q

In a cytotoxic brain injury, what occurs?

A

The actual neurons will swell

144
Q

What is normal intracranial pressure?

A

0-15mm Hg

145
Q

What is the formula for ICP (The monro-kellie hypothesis)?

A

Brain tissue + CSF Volume +Blood Volume

146
Q

What is CPP?

A

Cerebral Perfusion Pressure

It measures the adequacy of capillary hydrostatic pressure pushing nutrients out of the brain tissue

147
Q

What is the formula for CPP?

A

CPP=MAP - ICP

148
Q

What is a normal CPP?

A

70-100 mmHg

149
Q

What are some of the causes of increased ICP?

A

Increased brain tissue (Tumors, cerebral edema)
Increased CSF volume (Excess CSF production or decreased CSF drainage)
Cerebral Bleeding (Traumatic bleeds, burst aneurysms, etc)

150
Q

What are the manifestations of Increased intracellular pressure?

A

Sustained increased ICP causes hypoxic injury
Change of consiousness most sensitive indication***

Very late sign: CNS ischemic response “Cushing’s reflex” or “cushing’s triad”

Eventual death of neurons

151
Q

What is herniation of the brain?

A

Displacement of brain tissue due to increase ICP from area of higher pressure to lower pressure

152
Q

What are the manifestations of brain herniation?

A

Specific manifestations depend on what portion of the brain herniates

Motor, respiratory or pupillary diysfunction
May be unilateral or bilateral
Posturing, eventual coma

153
Q

What is hydrocephalus?

A

An increase in CSF volume that eventually enlarges the ventricles that may occur from:
-an overproduction of CSF
-impaired reabsorption of CSF through arachnoid villi

154
Q

The severity of hydrocephalus depends on?

A

The speed of development

155
Q

What is the leading cause of death from brain injuries in <24 year olds?

A

TBI

156
Q

The blunt trauma (normally caused by a MVA) causes general injury by?

A

The sudden deceleration causes coup and contrecoup injuries
-tissue and vessel swelling possible

The secondary swelling, edema and ischemia begin soon after and lead to ICP related problems

157
Q

What is a coup brain injury?

A

A bruise directly related to the trauma at the site of impact

158
Q

What is a contracoup brain injury?

A

A contracoup brain injury involves a contusion remote from, and classically opposite to, the actual site of impact to the head

Caused by the secondary impact

159
Q

What are the primary TBI injuries due to?

A

Focal Lesions: contusions, hemorrhage
Diffuse injuries: Concussion, diffuse axonal injury

160
Q

What are the secondary TBI injuries due to?

A

Brain swelling
Infection
Ischemia/hypoxia

161
Q

A mild brain injury that can result from a blow to the head, a MVA, or shaking that may have a brief loss of consciousness is called?

A

A concussion

162
Q

What are some of the manifestations of a concussion?

A

A person may have amnesia surrounding the injury and extended confusion

Postconcussion syndrome involves confusion, headache, dizziness, sleep problems lasting from days to weeks

Cumulative effect of multiple concussions

163
Q

What is considered a moderate brain injury?

A

A brain injury with more extensive vascular damage that causes:
-loss of consciousness
-cognitive and motor deficits possible
-contusions are often visible on CT

164
Q

What is considered a severe brain injury?

A

A brain injury that has significant mechanical damage
Often causing hemorrhages
Significant neuro deficits and loss of function

165
Q

Where do epidural hematomas occur?

A

Usually in the parietal or temporal lobes, often following a skull fracture.
However, these do not cross lobes

166
Q

An epidural hematoma often follows?

A

A TBI severe enough to cause loss of consciousness

167
Q

What occurs during an epidural hematoma?

A

The affected lobe is forced downward/inward by growing hematoma
The ICP gradually increases to a severely high level causing herniation to occur
The Pt. quickly loses consciousness again

168
Q

What is a subdural hematoma?

A

A subdural hematoma is often caused by a tear in bridging veins on the surface of the cortex that can involve more than one lobe

169
Q

When will signs and symptoms of a acute subdural hematoma occur?

A

Signs and symptoms will occur within 24 hours of injury

170
Q

When will signs and symptoms of a subacute subdural hematoma occur?

A

Signs and symptoms will occue 2-10 days after the injury

171
Q

When will signs and symptoms of a chronic subdural hematoma occur?

A

They may take several weeks to appear

172
Q

Traumatic intracerebral hematomas are?

A

Single or multi-side bleeds following a TBI that are more likely in elderly adults and persons with excessive alcohol use

173
Q

What are the manifestations of traumatic intracerebral hematomas?

A

Manifestations depend on number, size, and location of bleeds

174
Q

What percentage of cardiac output is cerebral blood flow?

A

15-20%

175
Q

What is the MAP of cerebral autoregulation of blood flow?

A

between 60-140

176
Q

What gas concentrations effect cerebral blood flow?

A

CO2, H+, O2

177
Q

What occurs after several seconds of interruption to cerebral blood flow?
What about in 4-6 minutes?

A

Several seconds of interruption will cause unconsciousness

Irreversible damage occurs after 4-6 minutes if interruption

178
Q

What is a stroke?

A

An acute brain injury that is due to a vascular disorder

179
Q

What are the vascular disorders that can lead to a stroke?

A

Vessel Disease (atherosclerosis)
General decreased perfusion
A clot interupting blood flow
Vascular rupture

180
Q

What is the third most common cause of death, and also a major cause of disabilities?

A

Strokes

181
Q

What demographic are strokes more common?

A

More common in black people 65 and older

182
Q

What state is called the ‘stroke belt’?

A

SC

183
Q

What are the risk factors for strokes?

A

Increasing age
Male gender
Non-white ethnicity
Smoking
HTN
Cardiac Disease
Family History

184
Q

What percentage of strokes are caused by interruption of cerebral blood flow?

A

Ischemic strokes make up 85-90% of strokes

185
Q

What percentage of strokes are caused due to hemorrhage of a cerebral vessel?

A

10-15% of strokes are hemorrhagic

186
Q

What is an ischemic stroke?

A

A blockage of blood flow through a cranial artery due to a narrowing, blockage or vasospasm that are normally not painful

187
Q

What are the two types of ischemic strokes?

A

Thrombotic Type
Embolic Type

188
Q

What is a thrombotic type stroke?

A

A clot may develop locally at site of atherosclerosis, or clot may travel ‘downstream’ and lodge distally

189
Q

What is a embolic type stroke?

A

A blood clot from somewhere else in the body (usually LV or carotid arteries) travels to the brain

190
Q

What type of window do strokes have for treatment?

A

A brief window

191
Q

What occurs when someone is experiencing an Ischemic stroke?

A

When the CBF is <20% of normal infarction occurs.
-Tissue forms around ischemic core
-Surrounding ischemic core is the ‘pneumbra’
-Loss of blood supply depletes ATP production
-Na/K pump fails and causes cell swelling
-Neurotransmitters released
-neuronal injury and death occur

192
Q

What is the ‘penumbra’ surrounding the ischemic core?

A

Cells that are impaired but can be saved if circulation is returned

193
Q

What are the manifestations of an ischemic stroke?

A

Vision loss
Unilateral numbness/weakness
Loss of Balance
Sudden confusion
Loss of speech
Loss of swallow/gag reflex

**specific deficits depend on location of lesions or blockages

194
Q

What are the most common results of an ischemic stroke?

A

Motor deficits (on contralateral side) then language deficits are most common results

195
Q

What is a transient ischemic stroke?

A

Preludes to ischemic stroke caused by a treatable cause if the cause is identified.
The brain tissue is injured but not dead and neurological deficits resolve around an hour

Often due to atherosclerosis of carotid artery.

196
Q

A greater frequency of ___________ __________ __________ strongly predicts a future ischemic stroke.

A

Transient ischemic strokes

197
Q

What is a hemorrhagic stroke?

A

A stroke that can be intracerebral or sucarachnoid that is caused by a rupture of a cranial vessel often pre-existing a cerebral aneursysm

198
Q

What is a huge risk factor for a hemorrhagic stroke?

A

HTN

199
Q

Which has greater mortality rates, an ischemic or a hemorrhagic stroke?

A

Hemorrhagic

200
Q

______________ _______________ rapidly worsen due to increased ICP from bleeding during hemorrhagic strokes.

A

Neurological symptoms

201
Q

If there is a large bleed during a hemorrhagic stroke, what occurs?
What about a small bleed?

A

Large Bleed: Rapid unconsciousness
Small Bleed: Severe headache sometimes described as “worst headache ever” and vomiting is also common

202
Q

What is the treatment for a ischemic stroke?

A

Quick reperfusion of brain tissue with thrombolytic drugs or mechanical disruption of the clot through a catheter

203
Q

What is the treatment for a hemorrhagic stroke?

A

Surgical treatment or drugs may be used to manage arterial and intracranial pressure, clotting factors may slow bleeding

204
Q

What are two CNS infections?

A

Meningitis
Encephalitis
Commonly due to bacteria, viruses or fungi

205
Q

What is Meningitis?

A

Inflammation usually due to infection of the pia mater, the arachnoid and the subarachnoid space

206
Q

What is encephalitis?

A

inflammation of the brain parenchyma

207
Q

What is the pathophysiology behind meningitis?

A

A bacteria invades CSF releasing endotoxins

Endotoxins stimulate inflammatory mediators of the meninges

Neutrophils arrive, bind to and damage the endothelial cells of BBB

BBB damage allows fluid and more pathogens to move across capillary walls CSF

Vessels within the meninges become inflammed and dilated increasing volume and viscosity of CSF->Increased ICP

208
Q

What are the manifestations of bacterial meningitis?

A

Headache
Photophobia
Nuchal Rigidity
Fever
Pain through body
Nausea/vomiting

209
Q

What is the diagnostic test for bacterial meningitis?

A

A lumbar puncture-CSF will be cloudy, purulent, reduced glucose levels and pressure will be higher than normal

210
Q

What are the 3 bacterial potential causes of bacterial meningitis?

A

Neisseria meningitidis
Streptococcus pneumonia
H. Influenza

211
Q

What are some additional signs and symptoms if the cause of the bacterial meningitis is from meningococcal menigitis?

A

Rash on extremities
Possible gangrene
Organ failure

212
Q

What type of meningitis is generally less severe than bacterial meningitis and is often self limiting?

A

Viral meningitis

213
Q

What is the CSF makeup if infected with viral meningitis?

A

CSF contains mainly lymphocytes, moderately elevated protein, and glucose is normal

214
Q

What is encephalitis?

A

A generalized infection of parenchyma of brain and spinal cord causing edema, necrosis, and breakdown of neurons

215
Q

What are the common causes of encephalitis?

A

Herpes Simplex Virus
West nile virus
Rabies Virus
HIV

Other causes can be bacteria and fungi

216
Q

What are the signs and symptoms of encephalitis?

A

Fever
HA
Nuchal rigidity
LOC changes

217
Q

1 in 10 people will have at least one ________________ in their lifetime.

A

seizure

218
Q

What is the cause of a seizure?

A

Excessive activity of neurons in the brain especially the paroxymal discharge of cerebral neurons

219
Q

What is epilepsy?

A

Disorder of repeated, idiopathic seizures

220
Q

What are the problems with seizures on the cellular level?

A

Membrane instability
Hypersensitive neurons
Neurotransmitter or electrolyte imbalances

221
Q

What are focal seizures?

A

Seizures that start in a specific area of the brain

222
Q

What are the two types of focal seizures?

A

Focal without impairment of consciousness

Focal with impairment of consciousness

223
Q

Focal seizures without impairment of consciousness are?

A

Focal seizures where the person maintains consciousness but may have small motor or sensory effects (aura)

224
Q

Focal seizures with impairment of consciouness are?

A

Consciousness is impaired or lost, more likely to have visible motor effects and confusion following

225
Q

What is the timeline for generalized seizures?

A

Begins with both hemispheres at the start and loss of consciousness immediatley
-tonic-clonic: rapid loss of consciousness, falls to ground, jerking of whole body, loss of bladder/bowel dunction

-postictal period

-absence: No convulsions, brief alteration of consciousness, common in children

226
Q

What is Status epilepticus?

A

Continued seizure activity that doesn’t resolve on it’s own and is generally labeled SE after about 10-20 minutes and is considered an emergency

227
Q

What are the complications of status epilepticus?

A

Hyperpyrexia
Bronchial obstruction
Aspiriation of vomitus
Breakdown of cardiovascular function

228
Q

Neurocognitive disorders are?`

A

An updated term for dementia that involves a decline in mental function that is not a normal part of again, severe enough to interfere with overall function

229
Q

What are some common examples of neurocognitive disorders?

A

Delirium
Alzheimer Disease
Vascular disorders
TBIs
Parkinsons
Huntington Disease
HIV
Substance abuse

230
Q

What is delirum?

A

An acute neurocognitive disorder that has an increased risk with age and involves sudden loss of cognitive function, altered level of consciousness

231
Q

What are the causes for delirum?

A

Many different disease processes, such as medications and toxic substances

232
Q

What disease accounts for 60-80% of all NCDs?

A

Alzheimer Disease

233
Q

What are the potiential etiologies of Alzheimers Disease?

A

Genetics
Free Radical Damage
Inflammation

234
Q

What is the normal progression of Alzheimers Disease?

A

8-10 years

235
Q

What is the pathology causing Alzheimers?

A

-Abnormal levels of several neurotransmitters
-Lesions in neurons
-Gradual breakdown/loss of neurons in hippocampus and cerebral cortex that results in atrophy of the brain tissue and enlargement of the ventricles

236
Q

What type of lesions on the neurons are seem in Alzheimers?

A

Neurofibrillary tangles (distorted proteins)
Amyloid-beta plaques (Coat neurons)

237
Q

How is Alzheimer’s staged?

A

Stage 1-7

238
Q

Alzheimer’s Staging:
Stage 1

A

1-no impairment

forgetfulness

239
Q

Alzheimer’s Staging:
Stage 2

A

2-very mild
Occasional STM loss, aphasia, name recall problems

240
Q

Alzheimer’s Staging:
Stage 3

A

3-mild
About sx, more frequently

241
Q

Alzheimer’s Staging:
Stage 4

A

4-moderate
Above sx + periodic LTM problems, difficulty with complex tasks

242
Q

Alzheimer’s Staging:
Stage 5

A

5-moderatly severe
Disorientation, worsening LTM, innappropriate self care, decsions

243
Q

Alzheimer’s Staging:
Stage 6

A

6-Severe

Above sx, more frequent/severe
abnormal sleep, loss of sphincter control for bladder and bowels, worse dissociation from reality

244
Q

Alzheimer’s Staging:
Stage 7

A

7-very severe
Loss of most cognitive and motor control

245
Q

Renal disorders are classified by?

A

Site (upper or lower)
Degree (partial or complete)
Duration (acute or chronic)

246
Q

What are the causes of renal disorders?

A

Renal Calculi
Tumors
Clots
Pregnancy
BPH
Neurogenic bladder

247
Q

How does BPH cause renal disorders/obstruction?

A

The prostate gland in the 6th or 7th decade of life can begin to enlarge and the gland wraps around the urethra, squeezing it off and causing an obstruction

248
Q

Urinary obstructions:
What would be an example of a internal blockage?

A

A kidney stone

249
Q

Urinary obstructions:
What would be an example of an external obstruction?

A

Pregnancy
Tumors

250
Q

Urinary obstructions:
What would be an example of a partial obstruction?

A

Scar tissue

251
Q

The effects of a urinary obstruction depend on?

A

the effects depend on unilateral/bilateral and degree of obstruction because they determine the backflow direction.
Ex: Bilateral obstructions will exhibit worse symptoms

252
Q

When a urinary obstruction occurs and the pressure in the ureter, renal pelvis and tubules occurs, what are the pathological risks?

A

The stasis of urine can increase the risk of infection.
Structural damage can occur due to the dilation of the urinary tract and hydronephrosis
Eventually kidneys and nephrons can atrophy

253
Q

What is hydronephrosis?

A

excess fluid in a kidney due to a backup of urine.
(Stretching/damage in the kidney)

254
Q

For filtration to occur during urine production, what pressure gradients are needed?

What occurs is the pressure gradient is not present?

A

High pressure is needed in the glomerulus and low pressure is needed in bowman’s capsule

Urine production will come to a halt if the pressure gradient isn’t right

255
Q

What is the the condition known as hydroureter?

A

Stretching/damage in the ureter due to a blockage

256
Q

Ongoing obstruction of urine can cause?

A

Permanent structural changes within the urinary tract such as hydroureter and hydronephrosis leading to eventual atrophy if blockage is not corrected

257
Q

What is the most common cause of upper urinary tract infections?

A

Renal calculi (nephrolithiasis)

258
Q

What are crystalline structures the develop when urine is concentrated with ions and a nucleus forms?

A

Renal calculi

259
Q

What are the common ions that can cause renal calculi?

A

Calcium (80%)
Magnesium Ammonium Phosphate
Uric Acid
Cystine

260
Q

Staghorn renal calculi only develop when what occurs? Why?

A

“staghorn” or magnesium ammonium renal calcui form when a UTI is present because the presence of bacteria releases uriase which metabolizes these chemicals and forms stones

261
Q

Struvile stones are?

A

Made of magnesium ammonium phosphate and form in the renal pelvis, and grow inward, and are lso known as staghorn stones.

These can become very large

262
Q

What is the interventions for renal calculi?

A

Staying hydrated enough to allow stones to pass is the pain intervention

Pain medications given

263
Q

What are the risks for renal calculi formation?

A

Elevated calcium levels
-Parathyroid disorders (due to calcium)
-Bone diseases (breakdown/rebuilding ratio is off)
Long term immobility

264
Q

What are the manifestations of Nephrolithiasis (renal calculi)?

A

Pain usually in the flank area down the pubic area (may be colicky due to location of stone)

Diaphoresis

N/V

UA will likely show hematuria, possibly microscopic crystals

265
Q

What are the two types of urinary tract infections?

A

Lower/cystitus-bladder only
Upper/pyelonephritis-kidneys

266
Q

What are the organisms involved in urinary tract infections?

A

E. Coli (80%)
Enterococcus Faecalis
Klebsiella Pneumoniae
Proteus Mirabilis

267
Q

What are the risk factors for a lower urinary tract infection?

A

Female biological sex
-Sexual activity and pregnancy
Diabetes mellitus
Prostatitis
Neuromuscular disorders
Obstructions
Urethrovesical reflex
Indwelling catheters

For Snakes, Digging Prevents New Obstactles Underground Indefinetely.

268
Q

What is the Urethrovesical reflex?

A

The sphincter at the bottom of the bladder doesn’t close

269
Q

What are the manifestations of a lower UTI?

A

Frequency
Urgency
Possible cloudy urine
Dysuria
Suprapubic and lower back pain

**Very old/young have different symptoms

270
Q

What is the diagnostic criteria for a lower UTI on a urinanalysis?

A

Presence of >100,000 CFU/mL
Pyuria (presence of pus in urine)
Culture may be done to identify specific bacteria

271
Q

What is pyelonephritis?

A

Infection of the renal pelvis and interstitum

272
Q

What are the most common causes of Pyelonephritis?

A

Ascending UTI
Vesicoureteral reflux
Hematogenous spread of a bloodstream infection

273
Q

Is pyelonephritis usually unilateral or bilateral?

A

unilateral

274
Q

What is the vesicoureteral reflex?

A

A shorter than normal ureter changes the angle of insertion into the bladder.

Upon contraction of the detrusor muscle, the shorter ureter stays open and allows backflow of urine into the ureter

275
Q

Acute pyelonephritis is serious and patient should be monitored for signs of?

A

A systemic infection

276
Q

What are the manifestations of acute pyelonephritis?

A

Sudden onset of fever/chills
Myalgias (pain in groups of muscles)
Flank pain
N/V
Frequency and urgency
Tenderness at costovertebral angle
Urinary findings similar to UTI

277
Q

What is the definition of glomerular injuries?

A

Inflammation of or damage to the glomerular membrane usually due to an antibody-antigen reaction

278
Q

What are the non-immune causes of glomerular injuries?

A

Diabetes
Toxins
HTN
Genetic disorders

279
Q

What are the general manifestations of glomerular injuries?

A

Hematuria
Proteinuria
Decreased GFR
Edema
HTN

280
Q

What is the specific disease process that can cause nephritis that can occur within one to two weeks?

A

Acute postinfectious glomerulonephritis

281
Q

How are glomerular injuries named/categorized?

A

Usually named according to the appearance of the tissue, and categorized by their clinical manifestations that cause either nephritic or nephrotic syndromes

282
Q

What is acute nephritic syndrome?

A

A group of symptoms due to acute inflammatory processes where the lumen of the glomerular capillary becomes clogged with cellular debree and the capillary lining is damaged

283
Q

What does acute nephritic syndrome originate from?

A

It can originate from within and be limited to the kidneys or occur as secondary damage from a systemic disease

284
Q

What are the signs of acute nephritic syndrome?

A

Sudden hematuria
Mild/moderate proteinuria
Oliguria (reduced urine output)
Decreased GFR

285
Q

What is acute postinfectious glomerulophephritis?

A

Usually occurs (with greater incidence in children) after infection with a strain of GA Beta-hemolytic streptococci

286
Q

What is the pathophysiology of acute postinfectious glomerulophephritis?

A

Antibodies produced in response to the infection form complexes with antigens and capillary lumens become inflamed and congested by leukocytes and the glomerular basement membrane becomes inflamed.

TYPE 3 hypersensitivity reaction

287
Q

What are the manifestations of acute postinfectious glomerulonephritis?

A

Usually 7-12 days post infection from GA Beta-hemolytic streptococci

Hematuria (tea-colored urine)

RBC casts (Clumps)

Moderate proteinuria

Oligura

Edema

HTN

288
Q

Acute postinfectious glomerulonephritis is less likely to occur if?

A

Original infection is adequately treated

289
Q

What is the treatment for acute postinfectious glomerulonephritis?

A

Eliminate infection and provide supportive care

Recover in all ages in 6-8 weeks

*if not treated, inflammatory damage can occur in capillaries

290
Q

What is nephrotic syndrome?

A

A group of s/sx resulting from increased permeability of the glomerulus to proteins that can result from various disorders that damage the glomerular membrane

291
Q

In nephrotic syndrome, the larger ‘holes poked’ increases?

A

The leakage of bigger molecules into the urine

292
Q

What is the diagnostic criteria for nephrotic syndrome?

A

A 24 hour urine collection
-Fat molecules can be present (making urine appear cloudy)
-Albumin, complement proteins and globulins also can be found

293
Q

The hypoalbunemia from nephrotic syndrome can cause?

A

Fluid shifts to occur

(Think 3rd spacing and oncotic pressure)

294
Q

What are the signs and symptoms of nephrotic syndrome?

A

Significant proteinuria (>3.5 g/day)
Lipiduria
Reduction in urine output
Immune system effects
Coagulation cascade effected
Edema
Hyperlipidemia

295
Q

What is the relation between nephrotic syndrome and the liver?

A

The liver tries to compensate for lipid excretion, but overcompensates so we see elevated lipid levels

296
Q

Any rapid (<48 hours) decline in GFR indicates?

A

An acute kidney injury

297
Q

What is the mortality rate of acute kidney injuries?

A

25-80%

298
Q

What do acute kidney injuries cause?

A

Retention of metabolic waste products (azotemia) and electrolyte imbalances especially in Na & K+

299
Q

An acute kidney injury is usually accompanied by?

A

oliguria or Anuria

300
Q

How is an acute kidney injury classified?

A

By location of the problem

301
Q

Are acute kidney injuries treatable?

A

Yes, if caught quickly

302
Q

80-90% of Acute kidney injuries are?

A

Prerenal

303
Q

An acute kidney injury that has damage to the actual kidney is most likely a?

A

Intrarenal/intrinisic kidney injury

304
Q

An obstruction is most likely to cause which type of kidney injury?

A

Postrenal

305
Q

What are the causes of prerenal acute kidney injuries?

A

Short term:
hypovolemia
decreased cardiac output
Cardiogenic shock
Burns
Renal vascular obstruction

Drugs that decrease renal perfusion

Sometimes a localized issue such as a blood clot, but most (like above) are system issues

306
Q

What are the clinical manifestations of a prerenal acute kidney injury?

A

Oliguria
Increased BUN
Decreased GFR
Increased nitrogen

307
Q

All the issues causing prerenal acute kidney issues are mostly related to?

A

Perfusion
Decreasing BV, or BF

308
Q

In order for a prerenal acute kidney injury to stay in this stage, what must occur?

A

Problem needs to be treated within 48 hours or it will progress and damage will occur

309
Q

What are the causes of intrarenal acute kidney injuries?

A

Ischemia (due to perfusion past 48hr)
Acute tubular necrosis
Nephrotoxicity (Rx, contrast)
Inflammation (acute glomerulonephritis)
Toxemia of pregnancy
Malignant HTN
Rhabdomyolysis

310
Q

The clinical manifestations of an intrarenal acute kidney injury are?

A

Varied based off cause, stage, severity
but likely to see a decrease in urine output and rention of waste products

311
Q

What is the most common type of intrarenal acute kidney injury?

A

Acute tubular necrosis

312
Q

What is the etiology of acute tubular necrosis?

A

Ischemia of tubules
Septicemia
Drugs
Obstruction of tubules

313
Q

What occurs in acute tubular necrosis?

A

The epithelial lining of the tubules are destroyed and they slough off, blocking the tubules

314
Q

Acute tubular necrosis is reversible if?

A

Necrotic cells are removed

315
Q

What are the causes of postrenal acute kidney injuries?

A

Clots
Stones
Strictures
Tumors
BPH
Neurogenic Bladder
Trauma

316
Q

What are the clinical manifestations of postrenal acute kidney injuries?

A

Likely urinary retention
Eventual loss of pressure gradient at glomerulus that can decrease GFR

317
Q

What is the onset or initiation phase of an acute kidney injury?

A

The time between precipitating event and tubular injury that can be between hours and days

318
Q

What is the oliguric/anuric phase of an acute kidney injury?

A

Decrease in urine output/GFR and resulting problems that can occur between 1-2 weeks

319
Q

What is the diuretic phase of an acute kidney injury?

A

Kidneys begin to heal, urine output begins to return in 7-14 days

320
Q

What is the recovery phase of an acute kidney injury?

A

Gradual increase in urine output, SrCr decreases over several weeks

321
Q

What is chronic kidney disease?

A

Progressive loss of nephrons and decline in renal function lasting at least 3 months

322
Q

What does the destruction of nephrons do to the kidneys?

A

Affects all functins of the kidneys: fluid and acid/base balance, endocrine functions, elimination of waste.

Imp. Note-There is no restoration in kidney function once the kidneys are destroyed

323
Q

What are the common causes of chronic kidney disease?

A

Diabetes
HTN
Glomerularnephritis
Systemic autoimmune/inflammatory disorders
Congenital disorders

324
Q

All types of chronic kidney diseases cause?

A

A decrease in GFR

325
Q

What are the stages of chronic kidney disease?

A

Stages 1-5

326
Q

Stages of Chronic Kidney Disease:
Stage 1

A

Kidney damage with normal/increased GFR

GFR>/=90

327
Q

Stages of Chronic Kidney Disease:
Stage 2

A

Kidney damage with mild decrease in GFR

GFR=60-89

328
Q

Stages of Chronic Kidney Disease:
Stage 3

A

Moderate decrease in GFR

GFR=30-59

329
Q

Stages of Chronic Kidney Disease:
Stage 4

A

Severe decrease in GFR

GFR=15-29

330
Q

Stages of Chronic Kidney Disease:
Stage 5

A

Kidney Failure

GFR=15 (or dialysis)

331
Q

What is GFR calculated by?

A

Serum Creatinine
Age
Body Size
Gender

332
Q

GFR is inversely related to?

A

GFR is inversily related to serum creatine

333
Q

What is creatine?

A

Creatine is a molecule produced at a constant rate by the muscle and is filtered by the glomerulus

High creatine levels are the direct indicator that the GFR is going down.

334
Q

In addition to creatine, what other biomolecule is a huge indicator of a decreased filtration rate?

A

Protein in urine especially albumin

*Albumin is specifically an indicator of diabetic CKD

335
Q

What is microalbuminuria?

A

Small amounts of albumin in the urine, below the level of dectection of some tests

Marcoalbuminuria is larger amounts of albumin in the urine

336
Q

In Chronic kidney disease, due to the compensatory ability of the kidneys, CKD is often?

A

Silent until stage 3 or 4

337
Q

What is azotemia?

A

An accumulation of nitrogen wastes in the blood

338
Q

What is uremia?

A

Urine in the blood

339
Q

What are the uremic syndrome signs and symptoms from?

A

They are all due to the retention of nitrogen wastes in the blood

340
Q

In the early stages of chronic kidney disease, the kidneys?

A

lose their ability to regulate blood volume or concentrate the urine and therefore the urine may become isotonic to the plasma (the specific gravity is lower than normal)

341
Q

In the later stages of chronic kidney diseases, the kidneys?

A

have problems regulating sodium excretion and in most cases, eventual fluid volume overload occurs especially in stages 4 and 5.

Hyperkalmia also occurs

Pts. Trend towards metabolic acidosis

342
Q

________ of K + is excreted by the kidneys. In later CKD, how is this managed?

A

90%

In later CKD, most can be managed by dietary restriction

343
Q

In later CKD when patients trend towards metabolic acidosis, how does the body compensate?

A

The skeletal buffering system may minimize the acidosis, but bone density is lost

344
Q

What are the hematological effects of CKD?

A

Normochromic, normocytic anemia develops

Decrease in RBC lifespan due to extrinsic destruction from acidosis and azotemia

Platelet function is impaired causing bleeding risk

Synthetic EPO required in later stages by injection

345
Q

What are the cardiovascular effects of CKD?

A

**Major cause of death
HTN develops
Left ventricular hypertrophy
Dysrhythmias due to electrolyte imbalances

346
Q

What is the relationship between phosphate and calcium?

A

Phosphate is also excreted by the kidneys and there is an inverse relationship between the two.

347
Q

In CKD, why does hypocalcemia occur?

A

The reduced elimation of phosphate by the kidneys causes increased calcium excretion

348
Q

Where is Vitamin D activated?

A

In the kidney

349
Q

Why does secondary hyperparathyroidism occur in CKD?

A

Because of the hypocalcemia, the parathyroid secretes parathyroid hormone to increase calcium levels.

Calcium is taken from the mineralized bone, and bone density decreases

350
Q

What are the GI effects of CKD?

A

N/V
Altered sense of taste and smell due to uremia
Inflammation/ulceration of mouth and GI tract

NURS 709 Pathophysiology (5 decks)

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