Diabetes Management



Normal Blood Sugar


4-6 mmol/l






  • pallor

  • cool, moist skin

  • anxiety

  • restlessness

  • tingling in hands, feet tongue

  • confusion

  • drowsy

  • nausea






  • drowsy

  • confused

  • dry skin

  • nausea

  • headache

  • vomiting

Common Types of Insulin


Humulin R



Humulin N




onset 30-60 min

peak: 15-30min

duration 30-60 min






Duration: 24h

  • administered 30 prior to the first meal of the day

  • a second dose may be given before the evening meal or @ HS

  • may only be given Sub Q

  • may be given IV or subcutaneously

Do not mix







Duration: 24h


Meningitis and Encephalitis Comparision



Viral Meningitis Bacterial Meningitis Encephalitis
  1. Herpes Simplex
  2. Other
1. Haemopholis influenza – <5yrs2. Steptococcus pneumonia – adults3. Nesseria meningitis – youth
  1. Herpes Simplex
  2. Arboroviuses
  • Self resolution typical
  • HSV aggressive
  • Microbes replicate
  • toxins enter CSF
  • pus in subarachnoid space increases intracranial pressure
  • inflammation
  • purulent CSF
  • Localized necrosis and hemorrhage
  • edema
  • increased intracranial pressure
  • neural cell body death
  • neural fiber death
  • unpredictable progression
Normal glucose

Increased proteins


Low glucose

Increased proteins


Normal glucose

Increased proteins


  • Headache
  • fever
  • nuchal rigidity
  • emesis
  • nausea
  • Headache
  • fever
  • nuchal rigidity
  • emesis
  • nausea
  • Neural disturbances: stupor, coma, lethargy, seizures

  • Headache
  • fever
  • nuchal rigidity
  • emesis
  • nausea
Antivirals for herpes simplex

other viruses – typical self resolution



Antivirals for herpes simplex

Arbovirus – typical self resolution in 2wks

Wound Healing Pathophysiology


Phases of Wound healing

  1. Inflammatory Phase
  2. Proliferative Phase
  3. Remodelling Phase
  • duration of phases depends on the extent of injury and healing environment


Inflammatory Phase

  • inflammation occurs at time of injury
  • prepares wound environment for healing
  • blood vessel constriction
  • thrombus formation
  • vasodilation
  • increased capillary permeability
  • phagocyte emigration
  • digest debris
  • neutrophils arrive first, ingest bacteria, gone by day 3-4
  • macrophages appear 24hr after injury, remaining for an extended period
  • macrophages function in phagocytosis
  • macrophages release growth factors stimulating epithelial cells proliferation and angiogenesis
  • wounds may heal in absence of neutrophils, they cannot heal without macrophages

Proliferation Phase

  • begins within 2-3 days of healing
  • lasts up to 3wks
  • function – tissue building to fill wound space
  • fibroblasts produce collagen and other intracellular elements required for wound healing
  • 24-48hrs post injury fibroblasts and vascular endothelial cells begin proliferation of granular tissue (the foundation of scar tissue)
  • tissue is fragile and bleeds easily during to the # of newly formed capillary buds
  • in primary intention healing, epidermal cells seal the wound within 24-48h
  • epithelial cells require a moist surface for proliferation, therefore will wait to migrate under newly formed scab.
  • In cases of excessive granular tissue formation, re-epitheliarization may be impeded. Chemical cauterization may be required to allow healing to proceed
  • collagen synthesis peaks at 5-7days, continuing for several weeks

Remodelling Phase

  • 3 wks post injury, continuing 6 months or longer
  • cycle of collagen synthesis and collagenolysis
  • wound tensile strength increases
  • wounds will not regain original unwounded tensile strength
  • sutures provide 70% of tensile strength of non wounded skin
  • at suture removal 1 week post surgery, wound has only 10%
  • tensile strength increases to 70-80% over the next 4 wks before plateau

Factors Affecting wound healing

  1. Malnutrition
  2. blood flow & O2 delivery
  3. Impaired Inflammatory and Immune Response
  4. Infection, Wound separation and foreign bodies

Martin, Glenn and Porth, Carol, Mattson. 2009. Pathophysiology Concepts of Altered Health States. 8th ed. Lippincott Williams and Wilkins. Philadelphia

Helicobacter pylori and stomach ulcers


Stomach ulcers are caused by the gastric mucosa being infected with the bacterium Helicobacter pylori. Helicobacter pylori infects various areas of the stomach and duodenum causing inflammation and ulcers in the stomach.

There are two tests used to assay for the presence of H. pylori infection:

  1. Endoscopy where a tube with a camera is inserted down the esophagus into the duodenum to view the mucosal lining and obtain a tissue sample for assay.

2. The Ulcer Breath Test:

  • Carbon dioxide is exhale when we breath out
  • A breath sample is taken
  • Pranactin is then taken orally
  • A second breath sample is obtained once the Pranactin has been metabolised in the GI tract
  • The breath test is based on H. pylori’s ability to break down urea, the active ingredient in Pranactin.
  • H. pylori breaks down urea in a process that produces carbon dioxide.
  • The urea in Pranactin, however, is composed of a form of carbon called carbon 13, which is not found in high levels in breath.
  • When H. pylori breaks down the urea, carbon dioxide containing the carbon 13 is formed.
  • This carbon dioxide, containing carbon 13, enters the blood and travels to the lungs, where it is exhaled.
  • The test then compares first breath sample to the second sample and determines if a higher proportion of carbon dioxide (containing carbon 13) is present.
  • a higher level of carbon 13 in the second sample results in a positive H. pylori ulcer test.
  • Antibacterial medications to treat H. pylori infection can then be given

Martin, Glenn and Porth, Carol, Mattson. 2009. Pathophysiology Concepts of Altered Health States. 8th ed. Lippincott Williams and Wilkins. Philadelphia

Standard Precautions and Categories


Standard Precautions


An approach of infection control in which all human blood/body fluids or animals infected with infectious agents are treated as if known to be infectious from HIV, HBV, HCV and other bloodborne pathogens


Standard precautions are to be followed if there is a likelihood of coming in contact with:


  • blood

  • body fluids

  • secretions

  • excretions (except sweat)

  • broken skin

  • mucous membranes


When to Washing Hands:


  • between patients

  • after contact with blood, bodily fluids, excretions, secretions

  • contact with equipment or articles contaminated with them

  • immediately after gloves are removed


When to Wear gloves:


  • contact with blood

  • bodily fluids

  • secretions

  • excretions

  • broken skin

  • mucous membranes

  • contaminated items


When to wear masks, eye protection or face shields:


  • if care interaction may generate splash or spray of blood or other body fluids


When to gown


  • if clothing is likely to become soiled from blood or body fluids


  1. Client care equipment is sterilized, disposable single use items are discarded

  2. Contaminated linen placed in leak proof bag for laundry

  3. sharps disposed of in sharps container

  4. Single occupancy client room not necessary unless client hygiene unacceptable



Three Isolation Precautions Categories



  1. Air borne precautions


For known or suspected infections caused by microbes transmitted by airborne droplets

  • measles

  • chickenpox (varicella virus)

  • disseminated zoster

  • TB




  • private room – room door kept closed

  • negative pressure airflow of at least 6 exchanges per hour

  • respiratory protection device (N95 respirator worn for TB, varicella, disseminated zoster or measles and worker is not immune)

 2. Droplet precautions


For known or suspected infections caused by microbes transmitted by droplets produced by coughing, sneezing or talking


  • diphtheria (pharyngeal)

  • rubella

  • influenza

  • pertussis

  • mumps

  • mycoplasma pneumonia

  • meningococcal pneumonia

  • sepsis




  • private room or cohort clients (room door closed unless bed is more than 1m from the door)

  • mask is worn when within 1 m of the client

 3. Contact Precautions


For known or suspected infections caused by direct or indirect contact


  • colonization or infection with multidrug resistant organisms

  • C. difficile

  • major wound infections

  • gastrointestinal respiratory or skin infections

Perry, A, G, Potter, P, A, Ross-Kerr, J, C and Wood, M, J. 2006. Canadian fundamentals of nursing. 3rded. Toronto: Elselvier

The Universal Fatigue Assessment Scale


Phases of The Inflammatory Response


Phases of The Inflammatory Response


Vascular Phase

Cellular Phase: Leukocyte Margination, Adhersion and Transmigration

Leukocyte Activation and Phagocytosis Phase


  1. Vascular Phase


  • Characterized by changes in the small blood vessels @ the site of injury


  • Begins with momentary vasocontriction followed rapidly by vascodilation

  • Increases capillary blood flow

  • Results in: causes heat and erythema


  • Increases vascular permeability

  • Results in: causes protein-rich exudate emigration to tissues


  • Capillary osmotic pressure decreases with decreased intracapillary protein content


  • Interstitial osmotic pressure then increases

  • Results in: swelling, pain and impaired function


  • Decreased intracapillary volume results in decreased blood flow and clotting

  • Results in: localizing infection spread

 2. Cellular Phase: Leukocyte Margination, Adhersion and Transmigration


  • Leukocytes (mostly Neutrophils) delivered to site of injury

  • leukocytes then function in host defense


Leukocyte delivery is categorized by:

  • adhesion to capillary wall

  • margination – flattening cell to capillary wall

  • transmigration – squeezing though capillary wall

  • chemotaxis – following chemical gradient through tissues to injury site


Leukocyte recruitment to precapillary venules of injury facilitated by

  • slowing of blood flow

  • margination of leukocytes along vessel surface


Leukocyte adhesion and transmigration from the vascular space into the extracellular tissues is facilitated by:

  • complementary adhesion molecules (selectins and integrins) on leukocyte and endothelial surfaces

  • Leukocytes then migrate through tissues toward the site of injury by chemotaxis

 3. Leukocyte Activation and Phagocytosis


  • Ab binds foreign particle and receptor on phagocyte cell surface

  • Phagocyte engulfs Ab bound foreign particle

  • Phagocyte digests foreign particle


  1. Opsonization of microbe by complement factor and Ab facilitates recognition by neutrophil and Ab receptor

  2. Receptor activation triggers intracellular signalling and actin assembly in the neutrophil, leading to formation of pweudopods that envelop the microbe

  3. The phagocyte then fuses with an intracellular lysosome to form a phagosome into which lysosomal enzymes and oxygen radicals are released to kill and degrade the microbe


  • increased permeability of capiliaries

  • thrombocytes arrive, form clot

  • leukocytes arrange themselves along the endothelial lining – diaphoresis, move out into cellular tissue

Martin, Glenn and Porth, Carol, Mattson. 2009. Pathophysiology Concepts of Altered Health States. 8th ed. Lippincott Williams and Wilkins. Philadelphia

p.383 see diagram