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Top 100 Drugs > Final exam - study guide > Flashcards

Final exam - study guide Flashcards

1
Q

What are macromolecules?

A

> Macro = large

>ie. larger molecules like fats, carbs, and proteins

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2
Q

What is fat broken down into during catabolism?

A

Fatty acids and glycerol:

  1. triglycerides
  2. phospholipids
  3. cholesterol
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3
Q

Describe the properties/purposes of triglycerides

A

> 3 fatty acid chains attached to a glyceride molecule

> natural fats

> protect the internal organs - eg. the abdominal cavity has a fatty layer to protect the organs

> stores energy for fuel - when you cut carbs, fats are utilized

> insulates the body

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4
Q

Describe the properties/purposes of phospholipids

A

> 2 fatty acid chains and a phosphate group attached to a glyceride molecule

> AKA phosphoglycerides

> modified triglycerides

> a polar head (hydrophilic) and a non-polar (hydrophobic) tail - utilized in the cell membrane

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5
Q

Describe the properties/purposes of cholesterol

A

> ingested in animal products

> contains 4 interconnected carbon rings

> important for the stabilisation of cell membranes - the cell membrane is fluid and can move,cholesterol helps to anchor it

> used to synthesize steriod hormones, vitamin D, bill ena hormones from the adrenal cortex - without cholesterol there would be a reduction in these hormones

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6
Q

What are proteins broken down into during catabolism?

A

Amino acids:

  1. polypeptides
  2. enzymes
  3. vitamins & co-enzymes
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7
Q

Describe the properties/purposes of polypeptides

A

> short chains of amino acids

> eg. encephalins and endorphins are polypeptides produced by the body which can bind to receptors in the brain to provide temporary pain relief.

> eg. nonapeptides (made up of 9 chains of amino acids) like vasopressin and oxytocin are produced by the pituitary

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8
Q

Describe the properties/purposes of enzymes

A

> usually globular proteins - round shaped, water-soluble and used during metabolism

> their unique 3D shape needs to be maintained to allow binding to reacting molecules (substrates)

> are affected by pH, temp and some chemicals

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9
Q

Describe the properties/purposes of vitamins and co-enzymes

A

> can be water or fat soluble

> water soluble vitamins and not stored in the body but are required by many enzymes as a co-factor to carry out catalytic reactions.

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10
Q

What are carbohydrates broken down into during catabolism?

A

Glucose:

  1. monosaccharides
  2. disaccharides
  3. polysaccharides
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11
Q

Describe the properties/purposes of monosaccharides

A

> the smallest of the carbs - made up of 1 sugar molecule

> can combine to form disaccharides

> eg. glucose, fructose, galactose

> simple sugars that are readily absorbed into the capillaries and circulate through the digestive tract.

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12
Q

Describe the properties/purposes of disaccharides

A

> two monosaccharides are joined and a water molecule is removed

> too large to pass through a cell membrane

> broken down via hydrolysis - a water molecule is added to break the bond

> eg. lactose = glucose+galactose
eg.sucrose = glucose+fructose
eg. maltose = glucose+glucose

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13
Q

Discuss the function of fats in the body

A 
>insulation
>protection of major organs
>source of fuel after carbs
>help you to feel full when you eat
>used to build cell membranes
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14
Q

Discuss the function of proteins in the body

A

> make enzymes
make hormones
source of fuel after fats

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15
Q

Discuss the function of carbohydrates in the body

A

> main source of energy - ATP
regulation of BGL
sparing proteins and fats for other uses

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16
Q

What might alter the function of a protein and why?

A

> high temperatures - heat increases the kinetic energy causing molecules to vibrate so rapidly that the bonds are disrupted

> change in pH - ionic attraction disappears and the protein shape unfolds

> chemicals that alter the structure of enzymes

> radiation - can change the way a protein works and promote other diseases

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17
Q

Describe the vomiting reflex

A
  1. taking a deep breath
  2. closing the airways
  3. contracting the diaphragm and abdominal muscles
  4. relaxing the gastroeosophagle sphincter
18
Q

Describe the physiological alterations that may lead to vomiting

A

> severe pain

> distension of the stomach or duodenum

> trauma to the ovaries, testes, badder or kidneys

> ipecac (a medicine that causes vomiting) or copper salts in the duodenum

19
Q

What is vomiting?

A

> The forceful emptying of stomach contents and intestinal chyme through the mouth

> The vomiting reflex is triggered by stimulation of the vomiting centre in the brain

20
Q

Outline the clinical manifestations that you may observe in a patient who has experienced severe vomiting for several days.

A 
Long term vomiting can cause:
>dehydration
>alkalosis 
>damage teeth and esophagus 
>oesophageal cancer
>abscesses in the mouth
21
Q

Discuss possible causes of upper gastrointestinal bleeding.

A

> peptic ulcer disease
tears or inflammation in the esophagus
cancer of the stomach or esophagus
crohn’s disease

22
Q

Discuss possible complications that can result from upper gastrointestinal bleeding

A

> diarrhoea (blood is an irritant which increases peristalsis)
anaemia
elevated blood urea nitrogen due to digestion of blood proteins
hypovolaemic shock

23
Q

Discuss possible clinical manifestations of upper gastrointestinal bleeding

A

> haematemisis (vomiting blood)
occult blood (not apparent)
malena (blood coming out as they pass feces. Is usually black, smells foul)
haematochezia (bright red blood)

24
Q

What is the upper GIT

A 
>mouth 
>pharynx
>esophagus
>stomach
>duodenum
25
Q

Discuss the physical alterations that can lead to increased gastric acid production in the stomach.

A

> increase in the number of parietal/chief cells
decrease in inhibition of gastric secretions
increased sensitivity to food and other stimuli (eg. caffeine, histamine)
excessive vagal stimulation

26
Q

Discuss the physical alterations that can lead to

decreased mucous production in the stomach.

A

> Non-steroidal anti-inflammatory drugs (NSAIDS) which inhibit prostaglandin secretion resulting in decreased mucous production
lesions in the stomach caused by an overproduction of acid or pepsin in the stomach
inflammatory conditions (eg. inflammation caused by helicobacter pylori)
stress causing ulcersation
high alcohol consumption

27
Q

Discuss the treatments that could be used to alleviate symptoms observed in celiac disease.

A

> strict gluten-free diet leads to small bowel healing, resolution of symptoms, and a reduction in the long-term risk of these complications.
working with a dietician

28
Q

Discuss the treatments that could be used to alleviate symptoms observed in lactose intolerance.

A

> control diet - limit dairy/milk products
include small amounts of dairy into meals to build up a tolerance
Add a liquid or powder lactase enzyme to milk to break down the lactose
Using lactase enzyme tablets or drops before meals containing dairy can help to break down lactose

29
Q

Explain how the stomach protects itself from its gastric acid.

A

The mucosal barrier!

> the thick coating of bicarbonate rich mucus lining the stomach helps neutralize acid

> epithelial cells in the stomach’s mucosa are tightly
packed, blocking gastric acid from penetrating underlying tissue

> stem cells replace damaged epithelial mucosal cells

30
Q

What are the causes of osmotic diarrhoea?

A

> Lactase deficiency - where ingested lactose cannot be digested and hence absorbed in the small intestine

> Sorbitol - a non-absorbable synthetic sugar

31
Q

Describe the pathophysiology of osmotic diarrhoea.

A

Occurs when a substance in the intestine cannot be absorbed and instead draws water into the lumen via osmosis.

32
Q

What are the causes of secretory diarrhoea?

A

> excessive mucosal secretion of fluid and electrolytes,
inhibition of sodium chloride absorption
bacterial endotoxins (eg. cholera)
neoplasms (cancers) that produce hormones that stimulate intestinal secretions
gastrinoma
thyroid carcinoma
inflammatory bowel disease
Crohn’s disease
ulcerative colitis

33
Q

Describe the pathophysiology of secretory diarrhoea.

A

Occurs when electrolytes are secreted into the lumen, taking water with it.

34
Q

Describe the pathophysiology of a pneumothorax

A

The air enters the pleural cavity and separates the visceral and parietal pleurae, destroying negative pressure and causing the lung to collapse.

> primary - spontaneous (most commonly seen in young males)
secondary - caused by trauma (eg. fractured ribs, mechanical ventilation, COPD)

35
Q

Describe the S&S of a pneumothorax

A
  1. SOB/dyspnoea
  2. chest pain
>sharp chest pain during inhalation
>pressure in the chest
>cyanosis
>tachypnoea
>tachycardia
>shallow breathing
>decreased breath sounds/no breath sounds on the affected side
36
Q

Describe how the body would attempt to maintain homeostasis in a pneumothorax

A

> tachpnea - pressure prevents the lung from expanding so instead of long deep breaths, you take short shallow breaths

> tachycardia - HR then increases to compensate for the decreased O2 entering the body

> hypotension/decreased BP - increase HR means the heart doesn’t have as much time to fill the ventricles during relaxation, therefore on contraction, the force is not as strong

As nurses, we need to remove the air and reinflate the lungs.

37
Q

Describe the complications of a pneumothorax

A

> once you have a pneumothorax, it is easier to have another one.

> shock

> surgery may be needed to close the air leak.

38
Q

Describe the pathophysiology of emphysema

A

A form of COPD where the lung tissue around the alveoli are destroyed and we lose elastin. So instead of tiny little air sacs, we have inflated air sacs which reduces the surface area for gas exchange as well as makes it harder to hold the shape of the lungs for exhalation.

The major pathophysiologic change that leads to this widespread destruction is the excessive release of proteolytic enzymes from neutrophils and alveolar macrophages.

two pathophysiological changes that occur include:
>abnormal dilation of alveoli
>loss of lung elasticity

39
Q

Describe the S&S of emphysema

A 
>you will see hyperinflation on an X-Ray
>barrel chest
>frequent coughing/wheezing
>SOB
>tightness in the chest
>breathlessness
>pursed lip breathing
40
Q

How does the body compensate to maintain homeostasis during emphysema?

A

> Dynamic hyperinflation reduces SV since increases intrathoracic pressures and, consequently, decreases the preload by reducing both venous return and the volume of the left ventricle. As a consequence, there is a reduced filling of the left ventricle and consequently a reduced cardiac output

> kidneys retain bicarbonate to neutralise pH/overcome acidosis

> pulmonary hypertension - pulmonary artery pressure increases due to pulmonary vascular remodeling, caused by hypoxia, inflammation, and loss of capillaries in severe emphysema.

> tachypnea - to compensate for the damage to the air sacs resulting in less O2 entering the body,

41
Q

Describe the complications of emphysema

A

> Secondary polycythemia (abnormally high amount of red blood cells causing sluggish blood flow and an increased risk of clotting).

> Right heart failure - as the heart tries to pump blood into the damaged lungs, it can cause enlargement and strain on the right side of the heart that can lead to heart failure.

> blood clots - body may attempt to compensate for low oxygen level by increasing the number of RBCs. Sometimes, the increase in red blood cells can be so severe that it causes blood clots.

> Pneumothorax (escape of air from the lung into the pleural cavity).

> Respiratory failure– Often caused by acute infections of the lungs.

Top 100 Drugs (2 decks)

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