232 acute care Flashcards

(66 cards)

1
Q

progressive alterations to kidney function

risk level catergory serum creatinine, GFR and urine output

A

Increased Creatinine x 1.5
Decrease in GFR >25%

urine output
<0.5mL/Kg/hr
>6 hours

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2
Q

progressive alterations to kidney function

injury level catergory serum creatinine, GFR and urine output

A

Increased Creatinine x 2
Decrease in GFR >50%

urine output
<0.5mL/Kg/hr
>12 hours

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3
Q

progressive alterations to kidney function

faiure level catergory of serum creatinine, GFR and urine output

A

Increased Creatinine x 3
Decrease in GFR >75%

urine output
<0.3mL/Kg/hr
>24 hours or

Anuria >12 hours

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4
Q

progressive alterations to kidney function

loss level catergory serum creatinine, GFR and urine output

A

Complete loss of kidney function >4 weeks

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5
Q

progressive alterations to kidney function

end stage level catergory serum creatinine, GFR and urine output

A

End-stage kidney disease >3 months

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6
Q

classifications of acute kidney injury

A

prerenal
intrareal
post renal

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7
Q

Prerenal Acute Kidney Injury

A
Caused by impaired renal blood flow
Renal vasoconstriction
Hypotension
Hypovolaemia
Haemorrhage
Inadequate cardiac output
GFR declines because of a decrease in filtration pressure
Failure to restore blood volume or flow will cause irreversible cell injury
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8
Q

Intrarenal acute kidney injury

A

Intrarenal causes
Acute Tubular necrosis r/t prerenal kidney injury
Nephrotoxic acute tubular necrosis
Acute glomerulonephritis
Vascular disease – malignant hypertension, disseminated intravascular coagulation, renal vasculitis
Allograft rejection
Interstitial disease – drug allergy, infection, tumour growth

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9
Q

Acute Tubular necrosis

A

Caused by ischaemia
After surgery
Sepsis
Obstetric complications
Severe trauma including burns
Nephrotoxins (radiocontrast media, antibiotics)
Hypotension assoc. with hypovolaemia
Ischaemia generates free radicals that cause cell swelling, injury and necrosis
Reversible – depends on recovery of injured cells, removal of necrotic cells and intratubular casts, regeneration of tubular cells

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10
Q

Manifestations of ATN

A

Initiation Phase
Hours or days
Onset of causative event to tubular injury
Maintenance phase
Oliguric or non-oliguric Phase
Transition to oliguric – Decrease in GFR, retention of metabolic wastes (creatinine, urea and sulfate).
Urine output at lowest
Fluid retention – oedema, water intoxication and pulmonary congestion or oedema
Recovery phase
Repair of renal tissue takes place
Gradual increase in urine output, creatinine levels Fall

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11
Q

Postrenal acute kidney injury

A

Caused by urinary tract obstruction that places pressure on the kidney
Gradual decrease in GFR

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12
Q

Oliguria in AKI

A

Tubular obstruction theory
Necrosis of the tubules leads to sloughing cells and ischaemic oedema that obstructs the tubules. Backpressure leads to a reduction In GFR
Back-leak theory
GFR constant, tubular reabsorption of filtrate accelerated through alteration in permeability
Alterations to renal blood flow
Arteriolar vasoconstriction caused by release of angiotensin II, or blood moving from the cortex to the medulla. Autoregulation of blood flow impaired  decreased GFR.

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13
Q

kidney injury management principles

A
Correct fluid and electrolyte imbalances
Treat infections
Maintain nutrition
Monitor impact on medication regime
May require renal replacement therapy (haemodialysis)
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14
Q

what are the islets of langerhan

A

small clusters of endocrine tissue

Account for 2% of weight of pancreas

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15
Q

endocrine functions

A

Produce hormones secreted into bloodstream

Involved in nutrient balance (blood glucose levels) and gastrointestinal functions

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16
Q

what are the cells of the pancreas and what do they produce

A

Insulin produced by beta cells
Glucagon produced by alpha cells
Somatostatin by delta cells

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17
Q

Gluconeogenesis ?

A

– the formation of glucose, especially by the liver from carbohydrate sources such as amino acids and the glycerol portion of fats

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18
Q

Glycogenolysis ?

A

– breakdown of stored glucose to increase the blood glucose levels

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19
Q

Glucagon ?

A

– hormone produced by the alpha cells, stimulating the breakdown of glycogen in the liver, the formation of carbohydrates in the liver and the breakdown of lipids in both the liver and adipose tissue

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20
Q

main categorises for diabetes

A

Three main categories

Type 1 Diabetes Mellitus
Characterised by an absolute insulin deficiency

Type 2 Diabetes Mellitus
Insulin resistance with an accompanying deficiency in insulin production

Gestational Diabetes

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21
Q

describe type 1 diabetes

A

Autoimmune Destruction of the Beta (β) cells in the Islets of Langerhans

Severe or absolute lack of insulin caused by the loss of β cells

Slowly progressive autoimmune T-cell mediated disease that destroys the β cells

Concurrent abnormal production by alpha (α) cells with an increase production of glucagon.

Hyperglycaemia and ketonaemia can result from insulin deficiency however the excess of glucagon facilitates the other metabolic alterations seen in diabetes.

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22
Q

type 1 diabetes clinical maifestations

A
Classical Presentation
Polyphagia (increased hunger)
Polydipsia (increased thirst)
Polyuria (increased urine production)
Weight Loss
Ketoacidosis
Sweet Smelling Breath
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23
Q

type 1 diabetes assessment and management

A
Urinalysis
Presence of classic signs and symptoms
Management Aim
Avoid swings in insulin and glucose levels
Mimic body’s natural patterns
Monitoring Blood Glucose Levels
Long Term – Glycolated haemoglobin A1c 
The future
Islet cell transplantation
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24
Q

describe type 2 diabetes mellitus

A

Currently around 1.7 millions Australians have diabetes (of which 85% have Type 2 diabetes)

280 Australian develop diabetes every day (1 every 5 minutes)

Total annual cost in Australia is approx. $14.6 billion

Fastest growing chronic disease in Australia

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25
describe type 2 diabetes
Fasting hyperglycaemia occurs despite insulin being available Cellular Insulin resistance No ketoacidosis Gradual increase in hyperglycaemia Metabolic Abnormalities Insulin resistance Increased glucose production by the liver Impaired secretion of insulin by β cells
26
type 2 diabetes risk factors
History of diabetes in parents or siblings Obesity Physical inactivity Race/ethnicity
27
type 2 diabetes clinical manifestations
``` Slow onset Hyperglycaemia – polyuria and polydipsia Blurred vision Fatigue Paresthesia Skin infections ```
28
type 2 diabetes management
Changes in diet and exercise Hypoglycaemic medication possibly in combination with insulin
29
describe gestational diabetes
Occurs during pregnancy and resolves once the infant and the placenta have been delivered Glucose intolerance appears during pregnancy -New routine screening and screening of high risk women Family history of diabetes Some ethnic groups have a higher risk Advanced maternal age History of large babies Prior history of gestational diabetes or polycystic ovary syndrome Overweight prior to pregnancy (BMI >35) Women on corticosteroids or antipsychotics
30
complications of diabetes
``` Alterations in Blood Glucose Alterations in cardiovascular system Neuropathies Increased susceptibility to infection Peridontal disease ```
31
describe diabetes ketoacidosis
Four metabolic problems: - Hyperosmolality from hyperglycaemia and dehydration - Metabolic acidosis from an accumulation of ketoacids - Extracellular volume depletion from osmotic diuresis - Electrolyte imbalances (potassium and sodium) from osmotic diuresis Increased risk during physical or emotional stress – surgery, illness, infection, trauma, omitted insulin Occurs in Type 1 Diabetes
32
Diabetic Ketoacidosis – Manifestations and Treatment
``` Manifestations – flushed skin, increased thirst, fruity breath, decreased BP, increased HR, Kussmauls Respirations, confusion, Nausea, vomiting, abdominal pain, fatigue, weight loss, blurred vision Treatment Immediate medical intervention Primary Survey – Prioritise ABC IV hydration Regular Insulin Potassium Replacement Continuous cardiac monitoring ```
33
Describe the hyperosmolar hyperglycaemic state
Plasma Osmolality >340 mmol/kg Elevated Blood Glucose levels >33.3mmol/L Altered Levels of consciousness Precipitating Factors – infection, therapeutic agents or procedures, acute or chronic illness. Hyperglycaemia  increased urine output  plasma volume decreases and glomerular filtration rate decreases  glucose is retained and water lost  increase in glucose and sodium lead to increased serum osmolality  severe dehydration  intracellular water reduced in all tissue including brain
34
Describe the hyperosmolar hyperglycaemic state manifestation and Treatment
``` Manifestations - Flushed skin, increased thirst, decreased BP, increased HR, lethargic, nausea and vomiting, abdominal pain, fatigue, weight loss, malaise, extreme thirst, seizures Treatment Similar to DKA Primary Survey – ABCDE Intravenous fluid Potassium replacement Insulin administration ```
35
Hypoglycaemia - Manifestations
Autonomic nervous system- hunger, shakiness, nausea, irritability, anxiety, rapid pulse impaired cerebral function- strange or unusaual feeling, slurred speech, headache, blurred vision, decreasing levels of conciousness, difficulty thinking, inability to concentrate
36
Hypoglycaemia - Treatment
-Mild 15 g rapid acting or simple sugar (fruit juice, lollies, honey) Followed by a meal with complex carbohydrates Review diabetes management plan if occurring frequently -Severe Blood glucose <3mmol/L Conscious and alert – 10-15g of oral carbohydrate Altered consciousness – parenteral glucose or glucagon
37
host?
Host – any organism capable of supporting the nutritional and physical growth requirements of another organism
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Infection?
Infection – presence and multiplication of an organism within another living organism leading to injury to the host
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Colonisation ?
Colonisation – act of an organism establishing a presence in another organism
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Microflora?
Microflora – the harmless and normal bacteria that inhabits either internal or external surfaces of the human body
41
Mutualism?
Mutualism – an interaction where both the microorganism and the host benefit from the interaction
42
Parasitic Relationship?
Parasitic Relationship – infecting organism benefits from the relationship but the host either gains nothing or is harmed from the interaction
43
Infectious Disease?
Infectious Disease – is when the host sustains an injury from a parasitic relationship
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Virulence?
Virulence – the disease producing potential of the microorganism
45
Pathogens?
Pathogens – virulent microorganisms that are rarely found in the absence of disease
46
Saprophytes?
Saprophytes – organisms that obtain their growth from dead or decaying material in the environment
47
Opportunistic pathogens?
Opportunistic pathogens – produce infectious disease when the health and immunity of the host is weakened.
48
Agents of Infections Disease
Prions Creutzfeldt Jakob disease Viruses Bacteria Fungi - Yeasts – candida albicans - Moulds Parasites - Protozoa - Helminths – include nematodes (roundworms), cestodes (tapeworms) trematodes (flukes) - Anthropods –vectors of disease (ticks, mosquitos, biting flies) ectoparasites (mites-scabies, chiggers, lice-head, body or pubic and fleas)
49
Describe viruses
Classification Type of viral genome – either single or double stranded DNA or RNA Physical characteristics – size, presence or absence of a membrane envelope Mode of transmission – anthropod-borne viruses, enteroviruses Target tissue Type of disease produced Structure Enveloped viruses – enclosed within a lipoprotein envelope derived from the cell membrane of the parasitised host cell such as herpesvirus group, influenza and poxviruses
50
describe virus replication
Latent viruses – enter the host cell and insert their genome into the host cell chromosome where it remains in a latent state without causing disease Herpesvirus group – chicken pox, zoster, cold sores, genital herpes, infectious mononucleosis Retroviruses – after entry into the host cell, a viral enzyme translates the viral RNA into DNA. Viral DNA is integrated into the host chromosome where it exists in a latent state HIV – human immunodeficiency virus Oncogenic Viruses – transform host cells into malignant cells during replication Human papillomavirus
51
describe bactreria classification
Atmospheric conditions - Aerobes – require oxygen for growth and development - Anaerobes – cannot survive in an oxygen containing environment - Facultatively anaerobic – can adapt metabolism to either Staining - Gram-positive (stained purple by a primary basic dye)Streptococcus pyogenes - Gram-negative (not stained purple but counterstained red by a second dye) Legionella pneumophila - Acid-fast stain (resistant to the decolourisation of a primary stain when treated with a solution of acid alcohol) Mycobacterium tuberculosis Taxonomy -Classified into a small group of genetically related organisms (genus) and then further subdivided into individual species Staphylococcus (genus) aureus (species)
52
Portals of entry?
``` Penetration Direct Contact Vertical transmission Ingestion Inhalation ```
53
sources of infection?
-Endogenous vs exogenous Endogenous – acquired from hosts own microbial flora such as opportunistic infection) Exogenous – acquired from external environment such as water, food, soil etc - Carrier Human – mother to child transmission Inanimate object or fomite such as toys or tissues Zoonosis – animal to human transmission such as rabies from a bite or scratch - Place Hospital acquired (nosocomial) Community acquired - Body substance Blood, faeces, body fluids, respiratory secretions and urine
54
describe hospital inquired infection?
Acquired by individuals either during or immediately after a stay in a healthcare setting Either endogenous or exogenous Four Priority HAI (based on seriousness and associated costs - Surgical site infection - Staphylococcus aureus blood stream infection - Clostridium difficile infection - Central Line acquired blood stream infection MRSA – Methicillin-resistant Staphylococcus aureus
55
describe clinical presentation of infection
Localised Specific and reflect site of infection Diarrhoea, rash, convulsions, haemorrhage and pneumonia Systemic Nonspecific and shared Fever, myalgia, headache and lethargy Overt or covert
56
Describe different disease courses of infection
``` Incubation Period Prodromal stage Acute stage Convalescent stage Resolution stage ```
57
describe infection diagnosis
Culture – propagation of a microorganism outside of the body on artificial growth media - Identification based on microscopic appearance - Gram stain reaction - morphology Serology - Measuring serum antibodies in the diseased hosts
58
Treatment of Infectious Disease
``` Antibacterial Agents Antiviral Agents Antifungal agents Surgical Interventions -Drainage -Debridement -Removal ```
59
iv fluid administration steps
- 5 moments - 6 rights - follow chart and administration standard - open infusion set on tray - open tubing- make sure the roller is down prior to piercing the bag - pierce bag on clean flat surface - hang it up - squeeze the chamber gently 2-3 times, until it is about half way full - close the roller shut once the fluid has reached the end of the line. your line is now primed - in order to increase the drip rate, push the roller up. to decrease push roller down - follow drip rate calculation methods
60
how to prime an iv line manually, gravity
- look at med order and patient - look at bag for details, contamination, sedimentation or compromise - roller down, cap off and pierce bag - hang up on iv stand, prime by getting fluid into chamber - primed because there is fluid coming out -
61
why do we prime iv line
- to ensure no air can enter the venous circulation when line is attached to the patient at cannula
62
how to calculate iv dose
- giving sets are most commonly 20 drops/ ml (adults) and 60 drops/ ml (paediatrics) - to calculate drip rate in drops/ min (volume in hours) x (drop factor/ 60). refer to medsafe for practice - need to count that we are getting the correct amount to drops per min - connect bag to patient prior to counting drip rate. positioning cannula vein diameter. size of cannula may all effect drip rate.
63
how to do IDC male
-clean trolley -collect your equipment and start by opening the catheter pack onto the trolley surface - avoid contamination opening by using the corners of the pack - using whitre drape reposition the trays . allow space in the middle for other equipment - as drape is now contaminated it can be set aside and used during the procedure - pour chlorehexide or similar cleaning solution into one side of the tray with gauze - open lignocaine and place onto sterile field - place catheter onto sterile filed - remove gauze swabs from the opposite end of the tray, being careful to only make contact with the handle of the forceps -add 10 ml of water for injection (for inflating the balloon of the catheter) -open 10ml syringe onto sterile field for drawing up the water for injection repeat hand hygiene then don sterile gloves - draw 10ml of water for injection - carefully open drape then place over patient - bring over the tray containing chrhex soaked gauze swabs and lignocaine gel -using sterile drape from the pack carefully place around the penis ensuring your dominant hand stays uncontaminated - clean meatus using forceps, one swab at a time with a single downwards motion from anterior to posterior - use your towel to gently retract the foreskin to visualise meatus if necessary - lubricate external surface of the meatus using the lignocaine gel, then gently insert the nozzle into urethral meatus and slowly inject whole amount - hold the meatus closed keeping shaft vertical for 1-2 minutes to prevent gel from seeping out - place the tray holding the catheter and syringe containing WFI inbetween the patients legs on the sterile field - pick the catheter up approx 5-6 cm from the tip and introduce it into the meatus - gently advance catheter until urine is flowing. if you meet resistance do not force the catheter - you would usually advance the catheter all the way to the bifurcation and only inflate the balloon once urine is flowing - Reassure pt that almost done, observe signs of pain as balloon is inflating- if notice discomfort or pt says they feel pain DO NOT continue to inflate balloon, instead reposition catheter, ensure urine is flowing and try again -if foreskin was pulled back for insertion, ensure this is returned to normal position- if patient is able you can ask them to do this - dispose equipment, makr pt comfortable, document in pt notes- date time complications pain/ discomfort size and type of catheter used amount of water used to inflate balloon fluid balance chart add and stickers required by facility
64
what may cause resistance during male cathertisation
sometimes there may be slight resistance while catheter is moving past the prostate . cyou can ask patient to cough and take some deep breaths while you advance past it . it is important that your patient is as relaxed as possible during the procedure, so reassurance and distraction may be required
65
male catheter removal
non sterile gloves and 10 ml syringe to remove water inflating the balloon. attach the syringe to the port and allow the balloon to passively deflate then gently aspirate the syringe to ensure that the balloon deflation is complete ask your patient to take slow deep breasths and as the patient exhales gently remove the catheter. dispose according to facility policy
66
how to do female cathertisation
- hand hygiene - open cath pack on tray on tray - avoid contamination opening by using the corners of the pack - using whitre drape reposition the trays . allow space in the middle for other equipment - as drape is now contaminated it can be set aside and used during the procedure - pour chlorehexide or similar cleaning solution into one side of the tray with gauze - open lignocaine and place onto sterile field - explain procedure, gain consent, be aware of patients cultural needs and offer chaperone - check for latex allergy, position pt supine with knees bent, hips flexed and supported as necessary, feet apart or heels together ( if this is uncomfortable - left lateral side with right knee bent up - don sterile gloves and open sterile drape to place under patient between legs - be careful not to contaminate your sterile gloves when positioning the drape - draw up water for injection into 10ml syringe for inflating the balloon - squeeze lignocaine gel onto proximal 6cm of the catheter without nozzle touching the catheter, reserve half of the gel for inserting into urethra - bring tray with cleansing solution, gauze and lignocaine over to patient - using gauze to seperate the labia at the vulva with non dominant hand to expose the urethra - using forceps in dominant hand, clean meatus using one swab at a time, in a single downward motion from above the meatus down towards the anus - start at the outside working inwards, repeat until all 5 swabs are used and region is visibly clean - lubricate the external meatus using the gel syringe, then gently nozzle into the urethral meatus and inject gel and wait 3-5 minutes - bring tray with catheter over and place between patients legs - using dominant hand, pick up the catheter approx. 5-6cm from the tip and introduce it into the meatus in an upward and backward direction. gently advance till urine flow - ensure tray is close to patientso urine doesn't flow into bed - once urine is flowing , advance catheter further 6-7 cm and inflate the the balloon with water for injection - have drainage bag ready, and connect carefully without contaminating the open lumen. this is also a good time to collect a urine sample if required - withdraw catheter gently until resistance is felt - ensure pt is comfortable, cath is secure and clear equipment, discarding waste accordingly - document in pt notes- date time complications pain/ discomfort size and type of catheter/size, used amount of water used to inflate balloon, fluid balance chart add and stickers required by facility, urine characteristics determine plan of care for requency of urinanry measures and frequency of IDC changes