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129 Cards in this Set

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Limbic system

Controls emotional aspects of behaviour


Role is memory storage/recall


- related to dementia

Dementia

Cognitive decline


Not a normal part of aging


Short term memory loss, emotional stability, confusion


Due to loss/destruction of neurons


- usually caused by Alzheimer's

What can cause dementia?

Alzheimer's


Cerebro-vascular disease


CJD


Drugs

Alzheimer's

Form of dementia


If you can't find any cause


Generalized atrophy and degeneration of neurons


Age is greatest risk

Proteins wound up together in neurons

Neurofibrillary tangles


Pathological cause for Alzheimer's

Large proteins that can't be broken down


Different from neurofibrillary tangles


Outside of cells


Accumulates and forms plaques

Neuritic plaques


Pathological cause of Alzheimer's

Pathology for Alzheimer's

Cortex shrinks


Ventricles dilate


Progresses over 5-20 yrs

3 stages of dementia

Early


Middle


End

Early dementia

Hardest to diagnose


Forgetfulness


Communication difficulties


Mood changes


Requires minimal assistance


Middle dementia

Memory declines


Progressive cognitive impairments


Assistance with daily living


Behaviour change


Starting to lose ability to recognize people

End stage dementia

Unable to communicate


Requires total care


Chronic debilitation

What is usually the official cause of death for dementia sufferers?

Bronchopneumonia due to chronic debilitation

Pancreas

Produces "juice" that aids digestion


Soft gland, posterior to stomach


Tail reaches spleen


Made of aoini and pancreatic islets


Instrumental in diabetes

Glucose

Cells require this to make ATP


Nerve cells can't make or store glucose


Therefore needs it from the blood


Skeletal, fat, and liver cells can store glucose but need insulin to help facilitate

Which tissues do not require insulin for glucose delivery?

Brain, peripheral nerves, cardiac muscles and smooth muscles of the arteries

Hypoglycemia

Lack of glucose from the blood

Hyperglycemia

Too much glucose which can cause dysfunction and death

Insulin

Produced by beta cells in pancreatic islets


See a spike in insulin after eating

When does diabetes develop (3)?

1. No insulin is produced


2. Not enough insulin is produced


3. Insulin resistance

Diabetes Mellitus

"going through" & "honey sweet"


Sweet tasting urine


Group of disorders

Type 1 diabetes

Genetic


Complete lack of insulin because beta cells are destroyed by immune system


Hyperglycemia

Type 2 diabetes

Cast majority of cases


60-80% insulin resistance


High body glucose -} release more insulin -} decreased call response -} more insulin -} body cells respond



Will cause death of insulin-producing cells and fatigue

Functions of the digestive system (2)

1. Digestion


2. Absorption

Peristalsis

Motion of indegistive food in alimentary canal

Organs involved in diesgestion (3)

Liver


Gull bladder


Pancreas


Liver

Triangular, reddish-brown


In the right upper quadrant


4 lobes (usually all doing the same thing)

Functions of the liver (5)

Protection


Synthesis


Storage


Billiruben metabolism


Bile production

Liver failure: protection (4 characteristics)

-Hepatic portal vein drains nutrient rich venous blood from GI tract through liver



-Hepatocytes detoxify drugs, alcohol, pollutants, poisons



-Hepatocytes arranged into lobules



-Hepatic macrophages remove bacteria and debris from blood

Liver failure: storage

Stores vitamins


Amino acids (the ones we can't produce)


Iron


Lipids


Glycerin

Liver failure: Bilirubin metabolism

- damaged RBCs broken down by liver and spleen


- hemoglobin breaks down


- liver transfers bilirubin to bile, excretes bile to small intestines


- bilirubin eventually turns brown, which makes poop brown

Liver failure: synthesis

Hepatocytes produce variety of essential substances and waste


- plasma, proteins


- amino acids, cholesterol, fats


- bile


- urea (protein metabolism)

Hepatitis A (transmission)

Viral hep


Fecal-oral transmission


Contaminated water, food, milk, shellfish


Incubation period, 1 month

Hep B and C

Aka serum hep


Transmission through body fluids


Avg. 2-6 month incubation period


More severe


Liver becomes larger and edematous


Cell injury and necrosis

Cirrhosis

Permanent change to the structure of the liver


- chronic, irreversible, inflammatory

Manifestations of hepatitis

Mild, flu-like symptoms


Joint aches, low fever, nausea, fatigue, abdominal discomfort


Tender liver, skin rash, jaundice

Hepatitis - prognosis

Hep A - recovery in 6 wks with little long term side effects



Hep B + C - recovery in 8-10 wks


- more likely to be a carrier


- be chronic, or progress to cirrhosis or cancer

Cirrhosis - pathogenesis (4 stages)

1. Fat accumulates in cells


2. Bands of fibrous tissue from around lobules


3. Disorganized regenerative nodules form


4. Obstructed blood and bile flow

Manifestations of cirrhosis

Is due to portal hypertension or liver failure

Function of urinary system

Excretes water


Controls water, electrolyte, and acid balance


Regulates blood pressure by secreting remin (?)


Secrets erythropoietin (stimulates RBC)

Organs in urinary system

Kidney


Ureter - passage between kidneys and bladder


Bladder


Urethra

Kidney - cortex

Superficially outside

Kidney - medulla

Deeper layer, darker, made of renal pyramid

Kidney - nephron

In cortex, long tail extends down renal pyramid sending urine inwards


- the basic functional unit of the kidney


- 1 mill per person per kidney

Afferent arteriole

Blood supply for the kidneys

Kidneys - Glomerulus

Capillary bed in ball shape


No gas exchange happens here

Kidney - peritubular capillary

Drains away to renal vein and back to heart

Kidney - Tubules

Capsules that surround the glomerulus and captures any fluid that escapes



- Bowman's capsule/glomerular capsule

Urine formation (3)

3 processes:


1. Filtration


2. Reabsorption


3. Secretion

Urine - filtration

- Bowman's capsule surrounds glomerulus


- Blood comes in afferent arteriole


- Fluids and dissolved substances move through glomerular - membrane to Bowman's capsule


- driven by blood pressure


- throwing stuff out based on size


- energy efficient

Potocytes

Attach to outside of capillary

Glomerular filtration rate (GRR)

Fluid is filtered every 125ml/min


180L/day

Urine - reabsorption

Between peritube capillaries and internal structure


Return of useful substances to the blood


Water, glucose, amino acids, sodium, potassium


99% is reabsorbed

Urine - secretion

Movements of substances from blood to peritubular capillaries to the nephron tubules


- hydrogen, kreotene, hormones, drugs, etc.


- throw out more junk

Minor calyx

Urine secretion


Collect urine from nephron ducts


Point of triangle shape


Drains into renal pelvis


Into ureter


Stretch receptors are sensitive to filling in bladder


Sends signals to brain

2 types of nephron-related disease

Glomerular disorders


Eg. Glometonephritis



Tubular disorders


Eg. Pyleonophritis

Acute pyelonephritis

Infections of renal pelvis, calyces, medulla


Fecal-based like e. Coli


Usually through ureters but can enter from blood


Affects one or both kidneys

Manifestations of Acute pyelonephritis

Renal inflammation, edema


Infiltration of WBCs


Purulent urine


May lead to abscess and necrosis


Healing - scarring of tubules

Chronic Pyelonephritis

Even more scarring, recurrent auto-immune response to infection


Progresses to kidney failure

Glomerular disorders

From infections, toxins, immune responses


Proteinuria, decreased GFR


Low urine output


Edema, hypertension, higher blood volume, increasing blood pressure


Acute glomerulonephritis

Inflammation of glomeruli


Usually after fighting strep infection


Acute post-strep

- Abrupt onset 7-10 days after


- Bits of strep get stuck in the infiltration system membrane


- Attracts neutrophils and macrophages


- Will damage membrane


- Bowman's capsule leaks when it's not supposed to


-Fibrin (a clothing factor) doesn't clot properly and reduces urine


- blood and protein in pee


Lowered GFR


Hypertension


Edema in eyes, ascites


Usually resolvable without serious issue

Chronic post-strep

Just add scar tissue


Means reduced function and potential failure

Acute Renal Failure (ARF)

- Sudden drop in kidney function


- Often tubular necrosis


- Change to tubes themselves


- Ischemia


- nephrotoxic agents

Nephrotoxia

Kidney poisoning


Heavy metals


Organic solvents


Antifreeze


Antibiotics and pesticides

What causes ischemia in acute renal failure?

Hypovolemia (not enough blood)

Chronic renal failure (CRF)

Progressive and irreversible from loss of nephrons


Chronic glomerulonephritis


Chronic ischemia (leads to atrophy)

3 types ages of renal failure

- Based on percent of remaining kidney function


- must lose 75% to show symptoms


- will filter 15ml/min in end-stage


- may require dialysis


- fluid in brain

Normal flora

Usually in large intestines


More bacteria cells than human cells


Produce vitamins


Maintain water balance


Help fight pathogens

Pathogens

Organisms that cause disease


Normal flora are opportunistic pathogens


Could cause disease if they end up where they are not supposed to be


E. Coli


Strep

Types of microorganisms

Bacteria

Cellular - unicellular


Prokaryotes


Free-living (don't need a host)


Have a cell wall


Some have a slime wall


Some contain toxins


Reproduce very rapidly


3 main shapes of bacteria

Bacilli - pill


Cocci - circular (ie. Strep)


Spiral - syphillis

Viruses

Acellular


Simple structure


Capsid


DNA


Requires living cell host - won't replicate but may remain viable for hours or days


Usually tissue specific

Prions

Protein particle


Altered form of a normal host protein


Not broken down by enzymes


Progressively greater damage to neuron


Transmissible neurodegenerative disease


HCHO doesn't work


Aerosolization is major transmission

Example of prion

CJD


Slow progression


Non-inflammatory


Neuronal degeneration


Loss of coordination, dementia, death

Infection

When a microbe produces in body tissue


Step 1: transmission

Types of transmission (4)

Direct - touching a lesion


Indirect - involves intermediary eg. food


Droplet


Vector - insect or animal transmission

Fomite

Inanimate object that carries organisms

Pneumonia

Inflammation of lung tissue


Usually caused by bacteria


8th leading cause of death

How to classify pneumonia (3)

Infectious agent


Distribution (lobar, broncho-)


Source (community v. Hospital)

Bacterial pneumonia

Alveolar inflammation - fluid in alveoli from response


Most common in strep pneumonia


Onset depends on person's health


2 types of distribution: bronchial and lobar

Bronchopneumonia

Bronchial infected first


Spreads to adjacent alveoli


Patches of inflammation throughout lungs


Commonly in the chronic or terminally ill

Lobar pneumonia

Single lobe fills with exudate


Consolidation


Little residual damage


Healthy people fight it off with antibiotics


In compromised, exudate builds up


Breathing affected


Sepsis or death

Consolidation

Large areas fill with exudate


Accumulation of fluid, cells, tissue, or other material in alveoli


Attracts neutrophils into airways


Displaces air


Viral pneumonia

Atypical but happens in 50% of cases


No fluid buildup or neutrophils


Virus invades alveolar epithelium


Diffuse and bilateral

TB

Chronic bacterial infection caused by mycrobacterium TB (one specific type)


Affects those with decreased resistance from malnutrition and decreased immune response


Droplet


Aerobic bacteria - TB

Needs oxygen in order to grow efficiently


Has an extra thick slime layer and therefore more resistant


Constant ongoing response to try to isolate bacteria


Cause lesions can tubercles (granules)

TB - what happens to tubercles?

Centres grow and become Cassius necrosis


s


Scar tissue forms around and calcifiesisolated bacilliLesion is now a ghon focus


isolated bacilli


Lesion is now a ghon focus

What is a ghon complex - TB

If TB affects lymphnodes as well ghon focus

When can TB become reactive? (2)

1. Immune system impaired


2. Live bacilli escape to bronchi

What is different about secondary TB?

Lymphocytes jump in for secondary immune response


Faster with more necrosis


Widespread destruction of lungs


Cavitation


Localized in lung apex


Bleeding may happen

Flu

Acute upper respiratory tract infection from virus


Indirectly or droplet

Influenza type A

Affects proteins type H & N


Can insect multiple species

Influenza types B & C

Only infects humans


Milder, like a cold

Flu pathogenesis

Virus targets cells lining respiratory tract


Replicates until cell destroyed


Cellular injury and immune response


Very fast reaction

Sepsis

Life-threatening complication of infection


From any infection


Incidents is rising

4 stages of sepsis

SIRS


Sepsis


Severe sepsis


Septic shock

SIRS

Systemic inflammatory response syndrome

Sepsis

SIRS + infection

Severe sepsis

Sepsis + organ damage

Shock

Sepsis + hypertension


Not enough blood


50% mortality rate

Opioid

Painkillers


Body build up a tolerance

Fentanyl

Potent version of morphine (10x)


Used to bump potency of other drugs like heroin


Difficult to detect


So little is needed


Acts directly on brain stem


Inhibits respiratory centers in brain stem

2 types of head injury

Penetrating


Blunt

Cerebral concussion

No obvious evidence of brain damage


Temporary loss of consciousness


Vomiting


Headaches


Amnesia


Increased risk of chronic traumatic encephalopathy

Contusions

Bruising of brain


Rupture of small vessels near surface


Limb paralysis and decreased level of consciousness

Coup

On side where impact happened

Contrecoup

Rebound - head trauma

3 types of intercranial hemmorhage

1. Epidural hematoma


2. Subdural hematoma


3. Subarachnoid hematoma



Where hematoma= blood pocket

3 types of intercranial hemmorhage

1. Epidural hematoma


2. Subdural hematoma


3. Subarachnoid hematoma



Where hematoma= blood pocket

Layers of brain covering

Scalp


Meninges


Brain

Dura Mater


Thick mother


Superficial most layer

Arachnoid Mater

Spidey


A gap between this layer and the brain


Gap= subarachnoid space


Pia mater

Most inner most layer


Follows contour of the brain

Epidural hematoma

Between skull and Dura Mater


Collection of blood that won't even be touching the brain


Lack of consciousness sure to increased pressure on the brain

Subdural hematoma

Between Dura Mater and arachnoid Mater


Tearing of bridging veins


These drain to sinus


Bleeding is slower and limited in volume


Chronic or acute symptoms


- if chronic, symptoms are non-specific, dementia in elderly


Common in very young and very old



Subarachnoid hematoma

Between arachnoid and pia mater


Blood vessels on surface of brain


Or ruptured aneurysm

Flail chest

A type of thoracic trauma


Rib fractures


Paradoxical motion of the chest

Accumulations in pleural space

In membrane lining


Thoracic cavity wall sticks to the lungs and fixes them to the wall



Can be:


Blood


Air


Exudate


Water


Pus

Pneumothroax

Any Gas in pleural space


Very painful because of lung recoil


Can be from penetrating chest wound or spontaneous

Types of pneumothorax (2)

Open - rupture of lung lining itself


During sleep, rest, or exercise



Tension - mediastinal shift putting pressure on heart

Cirrhosis manifestations (4)

1. Portal hypertension - pressure causes hemmorhoids and esophageal varices


2. Liver failure - 80-90% of liver is destroyed

What happens during portal hypertension? (5)

Esophageal varices


Hemmorhoids


Caput medusae - varicose veins around intestine


Ascites


Splenomegaly - enlarges spleen

Portal circuit

Connects two capillary beds


Like from intestines/stomach to liver

What happens during liver failure? (6)

80-90% of liver is destroyed


Decreased albumin


Decreased clotting factors - bruising


Decreased hormone metabolism


Spider veins


Jaundice


Toxicity in brain


Pancreatic change in type 2 diabetes

Non-specific


Fat deposits


Enlargement


Progressive decrease in weight

Complications of diabetes (2)

Ketoacidosis - insulin deficiency - increased fat metabolism



Hypoglycemia- insulin shock


90% of type 1 cases

Diabetes - chronic complications (2)

Microvascular disease - retinopathy, damage to capillaries, neuropathy , kidney damage



Macro vascular disease like atherosclerosis



Peripheral vascular disease - gangrene



Neuropathies - nerve damage

Synergism

Lethal drugs become more potent with combo