the patient Flashcards

1
Q

What is teething?

A

first tooth usually erupts age 6 to 9 months

Full complement of milk, teeth by age, 2 1/2

It is normal and not an illness

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2
Q

Does teething cause a fever?

A

Some studies have shown a statistically significant rise in temperature about three days before tooth eruption

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3
Q

does teething cause of dribbling?

A

Saliva re glands start functioning at 2 to 3 months of age, which contributes to consistent dribbling

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4
Q

Does teething cause sleepless nights?

A

nocturnal awakening occurs at around eight months of age, when babies develop a sense of object permanence

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5
Q

Does teething, cause diarrhoea and cold symptoms?

A

At about six months of age, maternal antibodies start to decrease

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6
Q

What is non-pharmacological advice can you give for teething?

A

teething rings – some can be stored in the fridge, but can they be sterilised?

Wet, cold, flannel – to bite on

Chilled fruit/vegetable if a child is weaned. Beware of choking.

Extra cool water? Breast milk, ice lollies?

Protect from dribble rash

Clean teeth as soon as they come through and speak to dentist about first checkup

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7
Q

What is pharmacological help? Can you give me the symptoms of teething?

A

paracetamol/ibuprofen – at a suitable dose for age

Teething gels – not recommended as there is little evidence that they work

Be careful to avoid salicylate gels with reyes syndrome.

Teething gel is now behind chemist counter. Think about when you would sell them.

Homeopathic remedies claim to treat physiological symptoms and emotional issues associated with teething. Not recommended.

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8
Q

what is oropharyngeal candidiasis (oral thrush)

A

very young and very old

Identifiable risk factors
Broad spectrum antibiotic
Inhaled corticosteroids
Dentures
Nappy rash

Underlying pathology
Diabetes
Dry mouth
Immuno compromised

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9
Q

What are clinical features of oral thrush?

A

creamy white patches that can’t be right away, leaving a red raw mucosa

Spots of bleeding

Pain and altered taste can lead to a loss in appetite

Babies – do not feed well/nappy rash

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10
Q

treatment for oral thrush

A

miconazole - available OTC

Not for babies
Greater than four months, possible choking
not in Pregnancy

topical effect and systemic absorption
Interactions – warfarin enhanced affect

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11
Q

What is some advice for patients on the treatment of oral thrush?

A

councelling:
Use treatment for two days after symptoms have cleared.
daktarin gel can be used on the nipples of breastfeeding mothers
If using inhaled corticosteroids, use a spacer or rinse out mouth after using inhaler
dental hygiene and dentures – clean thoroughly at night, and then Rub with Daktarin gel
Babies – use of steriliser

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12
Q

red flags and danger symptoms with oral thrush?

A

diabetic patients
Duration greater than three weeks
Treatment failure
Immunocompromised patients
Painless patches
Unexplained numbness on lips and tongue
Changes in speech

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13
Q

what is leukopakia

A

usually a reaction to an irritant
White patch cannot be wiped off
Can also be a precancerous condition
Refer to a dentist immediately

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14
Q

what can mouth cancer be caused by

A

smoking
Alcohol
HPV

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15
Q

what are cold sores

A

herpes simplex virus

primary infection, normally in childhood
Virus enters through mucous membranes, lies dormant in the nerve root

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16
Q

What are the most common triggers of cold sores?

A

menstruation
Stress
Ultraviolet light
Extreme cold
Viral infections
Fever

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17
Q

What is the most effective use of cold sore treatment?

A

most effective if used early in an attack

Five times a day for five days
zovirax

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18
Q

What does a black hairy tongue mean?

A

bumps on your tongue Grow trapping bacteria

associated with poor oral hygiene, antibiotic use, smoking, drinking tea and coffee, and xerostomia

Try brushing/scraping tongue

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19
Q

what are mouth ulcers

A

Round, grey white with a red rim
less than 1 cm in diameter
Painful
Trauma/stress/tiredness
Hormone changes
Other medical conditions
Nutritional deficiency iron/B12

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20
Q

What is the treatment of mouth ulcers?

A

antiseptic
Anaesthetics
Corticosteroids
Saline, mouthwash

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21
Q

Medicines and medical conditions that can cause mouth ulcers

A

viral infections – chickenpox, cold sores, hand, foot and mouth disease

Crohn’s disease
Coeliac disease
Beta blockers
Chemo and radiotherapy
NSAIDs

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22
Q

what is angular chelitis

A

nutritional deficiency – B vitamins and iron and zinc
inflammatory skin disease
Infection
Windburn/sunburn
Licking lips

Treatments can depend on cause
Lip balm, if Winburn/sunburn
miconazole oral gel – antifungal and bacteriostatic
Talk about nutrition and refer to blood tests if necessary

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23
Q

Dietary advice to maintain oral health

A

do not consume sugar, two hours between meals
Sugar-free medicines
Never give pure fruit juice to children
Avoid sweetened dummies
water or Milk only in feeding bottles
Sugar-free gum after meals
Avoid acidic foods and drinks

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24
Q

what is xerostomia

A

dry mouth

Can be caused by:
Radiation
Damage/disease to salivary glands
antidepressants
Antihistamines
anti spasmodics

Can be helped by:
Frequent sips of water
Sucking ice cubes
Sugar-free gum
Artificial saliva

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25
Q

what is dyspepsia

A

overeating-GORD
Stomach irritation:
Food
Alcohol
Nicotine
Medicines – GORD

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26
Q

Symptoms experienced with dyspepsia

A

bloating feeling
Churning stomach
Stomach cramps
Discomfort/pain
Excess acid
Wind
Doll stomach ache

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27
Q

What is functional dyspepsia?

A

symptoms can include nausea/discomfort
Can occur after gastroenteritis/food poisoning
Normally acute but can become chronic
Epigastric, pain syndrome – interaction between nerves of the gut and central nervous system
Post prandial distress syndromes– problems with stomach, emptying relaxing

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28
Q

What is the treatment for functional dyspepsia?

A

diet – foods to avoid
Avoid stress/anxiety

drug therapy – PPIs – even though there may be no evidence that excess acid is involved

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29
Q

what is GORD heartburn causes

A

weekend/malfunctioning oesophageal sphincter
Pregnancy

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30
Q

GORD heartburn symptoms

A

severe pain in the upper chest
Burning in the back of the throat
Taste of acid
Burning pain rising to mouth
Excess acid
Sore throat/dry cough

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31
Q

Red flags/danger symptoms of heartburn

A

pain radiating down the arm
Cardiac problems
Pain radiating to the back or the shoulder
Pain waking up the patient
Patient is over 50
Bleeding
Weight loss
Anaemia
Assistant vomiting
dysphasia
Breathlessness and frequent symptoms

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32
Q

What is nonpharmacological advice for heartburn?

A

raise the bed or extra pillow to reduce symptoms at night

Stop smoking and reduce caffeine/alcohol intake

Decrease weight/low-fat diet

Avoid spicy/oily foods, or other foods that may trigger symptoms

Small, regular meals

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33
Q

What is treatment OTC for heartburn?

A

antacids
Magnesium salt
Aluminium salt
Sodium salt
Calcium salt

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34
Q

What is a proton pump inhibitor (OTC)

A

evidence that they are superior to H2 antagonists at controlling symptoms of heartburn

there are many drug interactions

If there is no relief of heartburn after two weeks, refer to GP

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35
Q

What are causes of constipation?

A

change of eating/lifestyle/routine
Ageing
Medication/other medical conditions
IBS
Pregnancy
Depression
Toddler constipation
Cancer (rare)

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36
Q

What is nonpharmacological advice for constipation?

A

increase fluid intake
Increase dietary fibre intake
Increase levels and frequency of physical activity
no delay in passing a motion

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37
Q

What are stimulant laxatives?

A

stimulate nerve endings in the gut
The increase peristalsis
Take 8 to 12 hours to work
Risk of lazy bowel
Caution in pregnancy

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38
Q

what are bulk forming laxatives?

A

same effect as increasing dietary fibre
Stool will be easier to pass as volume will be increased
must have an adequate fluid intake
Side effects can be flatulence and bloating

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39
Q

What are osmotic laxative?

A

where water is drawn into intestines

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40
Q

Describe signs of laxative abuse

A

buying large amount of laxatives
Buying laxatives on a regular basis

Physical signs:
thin
Pale clammy skin
Dry brittle hair
Dark circles around the eyes
Malnourished appearance

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41
Q

Red flags/danger symptoms of constipation

A

pain on defecation
Patient over 40, with a sudden change in habit with no cause
Duration of more than two weeks
Tiredness
Alternating constipation/diarrhoea (IBS?)
Substantial blood loss
dark tarry stools

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42
Q

What is haemorrhoids?

A

prolapsed anal cushions
rare under the age of about 20

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43
Q

What are the symptoms of haemorrhoids?

A

pain when passing motion with external haemorrhoids
Itching
Mucus discharge
Bleeding – bright, red, fresh blood

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44
Q

Risk factors of haemorrhoids

A

constipation
Straining
Being overweight
Lack of exercise
Heavy lifting
Those who stand or sit for long periods of time
Pregnancy or after child birth
Genetic disposition

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45
Q

What are treatment for haemorrhoids?

A

consider formulation – cream or ointment or suppository

Local anaesthetic – effect is short lived

anatrigents - little evidence they work

corticosteroids – hydrocortisone reduces swelling, and inflammation. Not in pregnancy. You have to be over 18.

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46
Q

Red flags/danger symptoms of haemorrhoids

A

Patient over 40 with sudden change in habits with no cause

Treatment failure

Patience, manually, reducing haemorrhoids

Severe pain

Blood mixed in with stool

Significance of bleeding

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47
Q

what are two types of viral diarrhoea

A

rotavirus
Norovirus

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48
Q

what is rotavirus

A

highly infectious virus resulting in 10% of children, and then up in hospital, due to dehydration

Vaccine introduced in 2013, and it has decreased cases by 70%

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49
Q

what is norovirus

A

winter vomiting bug
Small particles of vomit, or stores from person, getting in your mouth, contaminated, food, airborne, touching contaminated surfaces

Virus mutates, so no chance to get an immunity

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50
Q

Why is diarrhoea associated with travel?

A

cholera – bacterial infection
Typhoid – bacterial infection

Associated with severe diarrhoea, dehydration, dysentery (blood in stool)

Vaccinations are available for travel. Travellers should still follow personal/food hygiene advice.

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51
Q

Food hygiene advice for travellers

A

bottled water not tap
Sterilised tap water?
Food freshly prepared and hot
Avoid uncooked vegetables
Eat fruit, that can be peeled
Avoid ice cubes
Avoid locally produced ice cream/mayonnaise and other sauces

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52
Q

what is diarrhoea caused by protozoa (giardiasis)

A

caused by contaminated, drinking water aboard
always ask about foreign holidays when patients have diarrhoea
Watery, foul, smelling, diarrhoea, epigastric, pain, bloating, and wind
Refer to GPS suspected

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53
Q

Other less common causes of diarrhoea

A

anxiety
Food intolerance
Medication
IBS
Impaction

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54
Q

Oral rehydration therapy for diarrhoea (ORT)

A

glucose/rice powder with salt made up with water to form an isotonic solution

Often prescribed – check suitable ages over the counter

Make up with a 200 mL of plain water

Taken after each loose bowel movement

Discard if not drunk after 24 hours

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55
Q

treatment that is GSL and P for diarrhoea

A

loperamide

It’s reduces duration by 30 to 50%
It allows for reabsorption of fluid to take place
Should not be taken within 24 hours of fever, or if a bacterial cause of diarrhoea is suspected
age 12 and over – take two capsules initially, and one capsule after each episode of diarrhoea and up to 6 capsules in one day.

Side-effects include nausea, abdominal pain, drowsiness, dizziness, and dry mouth.

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56
Q

Non-pharmacological advice for diarrhoea

A

wash your hands thoroughly with soap and water after going to the toilet and before eating

Don’t prepare food for others

Clean the toilet, including the handle on the seat with disinfectant after each bout of diarrhoea

avoid sharing towels, flannels, cutlery

Don’t visit the people if unwell

Stay off work for two days after symptoms
have cleared

Avoid swimming pools for up to 2 weeks after diarrhoea

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57
Q

Red flag and dangerous symptoms of diarrhoea

A

medication such as diuretics
Patients are unable to drink
Change in bowel habit in patient over 50
Recent travel to tropical/subtropical climate
Blood or mucus in stool
Suspected impaction in children/elderly
Severe abdominal pain
Intolerance

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58
Q

Signs of dehydration in children and adults

A

feeling thirsty and lightheaded
Dry mouth
Passing water less than four times a day
Having dark coloured/strong, smelling urine
Passing urine, less often than usual

serious signs
Extreme Tiredness
Weak, rapid pulse
Dizziness that does not go away
Seizures

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59
Q

signs of dehydration in babies

A

Seem drowsy
Breathe fast
Have a few or no tears when they cry
Have a soft spot on the head that sinks inwards
Have a dry mouth
Have a dark yellow urine
How cold and blotchy looking hands and feet
Have not passed water in the last 12 hours

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60
Q

personal hygiene to prevent threadworms and parasitic worms

A

wear close-fitting underwear at night
remove in the bath and in the morning
Wear cotton gloves at night to avoid collecting eggs, when scratching
Wash hands and scrub under the nails regularly
Discourage nailbiting and finger sucking
Don’t share towels/flannels

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61
Q

Environmental hygiene to prevent threadworms and parasitic worms

A

vacuum and dust thoroughly
Wash toys
Throwaway Play-Doh
Change and wash clothes daily
Change and wash, bedlinen/towels, following treatment

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62
Q

Treatment for threadworms and parasitic worms
mebendazole

A

treat the whole family, even if not, all members are showing symptoms
Repeat treatment after 14 days to cover the whole life cycle
works by stopping the worm from absorbing glucose
There are interactions with anti-epileptics
Avoid in pregnancy
Suitable for children over 2

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63
Q

Red flags/danger symptoms when treating threadworms and parasitic worms

A

treatment failure
Secondary infection, due to scratching around the anus

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64
Q

What is the large intestine?

A

digested residues are further processed here
water and electrolytes absorbed
Leftover compact is to become stool

65
Q

How do we poo?

A

Peristatic waves move the stool into the sigmoid colon and rectum

Sensory nerves in rectum are stimulated

Individual becomes aware of the need to defecate

Stool moves into the anal canal, when the internal and external sphincters relax

66
Q

what is acute diarrhoea?

A

last for less than three days, probably due to an acute infection from Saturn pathogens, or from medications, with diarrhoea as a side effect

67
Q

What is chronic diarrhoea?

A

lasts for more than three days, probably due to several reasons. Could also be due to more severe problems such as ulcerative colitis

68
Q

What are some causes of diarrhoea?

A

norwalk virus
Rotavirus
Travellers diarrhoea
amoeba which causes amebiasis
Expired food
Side-effects of medications like antibiotics

69
Q

diarrhoea can be classed into three subtypes. What are these?

A

Secretory diarrhoea
osmotic diarrhoea
exudative diarrhoea

70
Q

what is exudative diarrhoea?

A

Due to chronic diseases

71
Q

What is osmotic diarrhoea?

A

Due to increased salt and sugar

72
Q

What is secretory diarrhoea?

A

Due to increased active secretion of mucus

73
Q

What is constipation?

A

happens when the stool remains in the large intestine for too long

74
Q

What can cause constipation?

A

in adequate diet
Infrequent exercise
Stress and anxiety
Suppression of the urge to defecate
Pregnancy

75
Q

What is the appendix?

A

A vestigial organ. Tubular in shape and about 8 cm long. The lumen joins the cecum

76
Q

what is IBS

A

Icronic gastrointestinal disorder of an unknown cause

20% of people experience it at some point in life

77
Q

Symptoms of IBS

A

abdominal pain or cramping
Diarrhoea or constipation
Flatulence
Bloated feeling
Feeling of incomplete bowel movement
Mucus in stool

78
Q

what is IBD

A

Inflammatory bowel disease

79
Q

Symptoms of IBD

A

abdominal pain or cramping
Bloody diarrhoea
Weight loss
Extreme tiredness

Inflammation of the got Crohn’s disease or ulcerative colitis

80
Q

what is an ostomy

A

Surgically creating an opening in the stomach in the abdominal wall for the elimination of dietary waste – maybe permanent or temporary

81
Q

what is a colostomy

A

a ostomy from a section of the colon

82
Q

what is a ileostomy

A

an ostomy from a section of the ileum

83
Q

What is the function of the kidney?

A

to remove waste products
Regulation of extra cellular fluid volume
Regulation of osmolarity
Regulation of ion balance
Regulation of pH
Production of hormones

84
Q

How is urine produced?

A

water and solutes from plasma
Nephrons of the kidneys
ureters
Bladder
Urethra
Excreted as urine

85
Q

Tell me about the nephrons

A

there are 10 million nephrons per kidney
80% are in the cortical
20% in the juxtamedullary
Juxtamedullary nephrons are important in producing concentrated urine
glomeruli all lie in the cortex

86
Q

What is the renal vascular system?

A

renal artery
Smaller arteries
Afferent arterioles
Capillaries of the glomerulus
Afferent arterioles
Peritubular capillaries
Venules and small veins
Renal vein

87
Q

What happens in the nephron?

A

excretion
Filtration and secretion
Reabsorption

88
Q

What is filtration?

A

movement of fluid and salute from blood into lumen of tubule
Plasma proteins and erythrocytes are not filtered
this occurs in the renal corpuscle
The glomerulus and Bowmans capsule

89
Q

what are the filtration barriers?

A

endothelium of glomerular capillaries
Basal lamina
The epithelium of Bowmans capsule

90
Q

How much plasma do the kidneys filter each day?

A

180 L

3 L of blood volume Approximately

1.5 L of urine is produced daily.

91
Q

what is the GFR

A

glomerular filtration rate
volume of plasma filters in a given time
Indication of how well kidneys are functioning
This is affected by:
Net filtration, pressure (blood pressure and blood flow)
Filtration, coefficient (surface area of capillaries and permeability)

92
Q

How do we regulate the GFR

A

auto regulation of renal blood pressure to maintain GFR over a range of systemic blood pressure

If the systemic blood pressure increases/decreases, then renal blood flow, increase/decrease

GFR will also increase/decrease if not regulated

93
Q

Regulation of GFR: myogenic response

A

an increased stretch of smooth muscle cells in the afferent arteriole (due to increased systemic blood pressure)

This triggers contraction of the afferent arteriole, thereby reduced blood flow. Maintaining GFR

If systemic blood pressure decreases afferent arteriole will dilate

94
Q

regulation of GFR: tubuloglomerular response

A

The distal convoluted tubule (DCT) runs between the afferent and efferent arterioles

specialise, macula, densa cells in DCT release paracrine factors. That act on juxtaglomerular cells in afferent arterioles

If flow increases in the distal convoluted tubule. Factors released to constrict afferent, arteriole

95
Q

Regulation of GFR: systemic hormones

A

angiotensin II is a vasoconstrictor
prostaglandin’s are vasodilators

96
Q

Regulation of GFR: sympathetic nervous system

A

its of a drop in blood pressure will result in an increased sympathetic output

Vasoconstriction of arterioles with reduce GFR and conserve fluid

97
Q

What is secretion?

A

movement of substances from plasma to tubular filtrate

Active transport of potassium, ions, hydrogen ions, organic acids, and bases, foreign substances, and metabolite

Uses selective membrane proteins to move molecules across the epithelium

98
Q

what is H+ secreted in for

A

Na+ in the PCT and DCT

99
Q

what is K+ secreted in exchange for

A

Na+ in the DCT and collecting duct

100
Q

what is reabsorption

A

99% of filtrate is reabsorbed
70% happens in the proximal convoluted tubule (PCT)
Fine regulation in the DCT and collecting duct

reabsorption is an active process, as filtrate is isosmotic with extra cellular fluid

It is driven by the sodium potassium pump and ATPase. On basolateral membrane of the tubular epithelial cells.

101
Q

Describe How re absorption occurs

A

sodium moves from the lumen into the epithelial cells down an electrochemical gradient

Pumped out of the cell into interstitial fluid against a concentration gradient

Water is reabsorbed by osmosis

Fluid moves from the interstitium into the capillaries due to low pressure in the capillaries

sodium linked, secondary active transport

Energy from sodium electrochemical gradient is used to move glucose into the epithelial cells against a concentration gradient

Facilitated diffusion of the carrier moves glucose out of the cell

102
Q

how are small proteins reabsorbed

A

trancytosis

103
Q

How can I active transport become saturated?

A

glucose carriers
Filtration is proportional to the plasma concentration
Reabsorption proportional to plasma concentration until maximum transport to rate is reached
Urinary excretion of glucose is evident above the threshold concentration

104
Q

Where is water reabsorbed?

A

In the descending loop of Henley

105
Q

Where are electrolytes reabsorbed?

A

in the ascending loop of Henley

Sodium ions, potassium, ions, and chloride ions

106
Q

Why is maintaining extra cellular fluid? (ECF) homeostasis important

A

maintains blood pressure and perfusion
Maintains cell integrity and function

coordinated by cardiovascular, respiratory, Renal and behavioural responses

Kidneys regulate sodium and water balance

107
Q

what is the role of the RAAS

A

it acts synergistically with the sympathetic nervous system to maintain blood pressure and tissue perfusion

It’s increases vascular tone
Stimulates aldosterone secretion
(Increases sodium retention)
Stimulates vasopressin (ADH) secretion
(Increases water retention)

108
Q

what are triggers for renin release

A

juxtaglomerular (JG) cells detect a drop in pressure in the afferent arterial

macula densa cells in distal tubule detect, a drop, infiltrate flow and sodium concentration

109
Q

what increases renin release?

A

prostaglandins

110
Q

what decreases renin release

A

adenosine

111
Q

what is ACE
angiotensin converting enzyme

A

membrane-bound enzyme on surface of endothelial cells

Peptidase – remove dipeptide units from C terminals at the end of peptides

inactivates other peptides, for example brandykinin

112
Q

what is the II-mediated affect?

A

vasoconstriction
Secretion of aldosterone from adrenal cortex
Increase in, nor adrenaline released from sympathetic nerve terminals
Cell growth
Increase sodium absorption from proximal tubule

113
Q

what is aldosterone

A

steroid hormones made in the adrenal cortex

It’s increases sodium reabsorption
Decrease is potassium, reabsorption

Release is increased by:
Decreased plasma osmolality
And increased plasma potassium ion concentration
angiotensin II

It’s acts on principle P cells in the distal tubule and collecting duct

It increases sodium reabsorption

It promotes excretion of potassium

114
Q

What is fluid and electrolyte homeostasis?

A

maintaining extracellular fluid (ECF), homeostasis important:
Maintains blood pressure and perfusion
Maintains sell integrity and function

Coordinated by cardiovascular, raspatory, renal and behavioural responses

Kidneys regulate sodium and water balance

115
Q

What is water balance?

A

kidneys conserve water
If fluid volume drops, less urine will be excreted

Urine osmolality can range from 50 to 1200 mOsm

It depends on the permeability of the collecting duct to water

116
Q

What is the countercurrent multiplier?

A

high osmolality of intestinal fluid of renal medulla is essential for water reabsorption

maintained by countercurrent multiplier action of the loop of Henley

Descending limb is permeable to water but not electrolytes

Filtrates becomes more concentrated descends from the core to the medulla

The ascending limb is impermeable to water, but actively reabsorbs electrolytes

Blood in the vasa recta flows in opposite directions to the filtrate in the tubule

The osmotic gradient is created by active transport of electrolytes from the ascending limb of the loop of Henley Is not diluted by water reabsorbed from the descending limb

117
Q

what is vasopressin

A

Its release is stimulated by the increase of plasma osmolality or decrease blood pressure/volume

it is released from the posterior pituitary

It acts on collecting duct cells to promote incision of aquaporin 2 water channels into Luminal membrane

It increases water permeability

It increases water reabsorption

118
Q

what is micturition

A

The bladder hold approximately 500 mL urine

Stretch receptors in bladder sends signals to the spinal cord

Reflex can be overridden by Imput from higher brain centres

119
Q

What does the GFR show us?

A

glomerular filtration rate

Volume of plasma, filtered in a given time (millilitres/min)

It is an indication of how well the kidneys are functioning

It is affected by:
Net filtration, pressure
Filtration, coefficient

120
Q

what is GFR and clearance

A

you cannot measure GFR directly
creatinine clearance: can be used to give estimate of renal function

It is the volume of plasma passing through the kidney, which has been totally cleared of creatine in a given time (ml/min)

Creatine as a product of muscle metabolism (it is filtered, but not reabsorbed, and very little is secreted)

121
Q

how do you calculate creatinine clearance?
(ClCr)

A

ClCr = excretion rate, creatine (mg/min) / plasma concentration, creatine (mg/ml)

a healthy adult ClCr is 125ml/min

122
Q

What is hypersensitivity?

A

unnecessary reactions to innocuous antigens
types I-IV

123
Q

What is auto immunity?

A

another set of chronic immune diseases

Auto immune diseases

It is a response to self antigens (autoantigens)
Mediated by autoreactive antibodies, and T cells
Antibodies can block normal physiology
T cells can damage healthy tissues

A failure of the immune system

An unwanted adaptive immune response against self antigens

Loss of tolerance

124
Q

What is tolerance?

A

it is a state of immunological on responsiveness to particular antigens

Requires education
Our immune system must learn what is self so that it can recognise non-self

125
Q

Mechanisms that contribute to immunological self tolerance

A

negative selection in the bone marrow, and thymus

Expression of tissue specific proteins in the thymus

No lymphocyte access to some tissues

Suppression of autoimmune responses by regulatory T cells

Induction of anenergy in autoreactive, Reactive B and T cells

126
Q

Describe B. Cell development – central tolerance

A

immature B. Cells in bone marrow:
no self reaction – migrate to periphery, mature B cell
Multi valent, self-antigen – clonal deletion - apoptosis
Soluble, self-antigen – migrate to periphery , aneroid B cell

127
Q

Describe T cell development – central tolerance

A

positive selection of T cells by cortical epithelial cells in the thymus

Negative selection of tea cells by dendritic cells, macrophages, and other cells in the thymus

128
Q

what are similar effector mechanisms to hypersensitivity

A

type II like
antibodies against cell/matrix antigen
Frequently directed at the blood cells

type III like
Immune complex mediated (soluble antigens)

type IV like
Effector, T cells mediated

IgE never causes autoimmunity

129
Q

what is autoimmune haemolytic anaemia

A

IgG and IgM bind red cells and activate complement
classical activation
Ab and C3b coated
removal of cells

130
Q

what is coombs test

A

Abs are shown attached to antigens on the RBC surface

131
Q

what is complement lysis

A

Where are part of the immune system causes the destruction or lysis of target cells. Particularly foreign cells or pathogens.

132
Q

What is the complement system?

A

A group of proteins that work together to defend the body against pathogens, clear, immune complexes, and supports various immune functions

133
Q

describe autoAbs to other blood cells

A

other blood cells are not so sensitive to compliment lysis
Clearance by phagocytosis

Neutrophils to neutropaenia

The white blood cell with antibodies and compliment can still function.
Treatment can be To slow their removal
splenectomy (to reduce clearance rate)

134
Q

what is organ specific

A

restricted effects
Targeted auto antigens in one or just a few tissues

135
Q

What is systemic?

A

multiple organs are affected
Widespread and varied autoantigens

136
Q

give organ specific examples

A

autoimmune disease of the thyroid
graves disease
Hyperthyroidism

Hashimoto’s
Hypothyroidism

137
Q

What is Graves’ disease?

A

normally:
TSH activates
release of T3/T4
block TSH release

autoimmune:
activating Ab to TSH receptor
Long, acting, thyroid, stimulating antibodies
T3&T4 unregulated release

Heat, intolerance, nervousness, weight loss, enlargement of the thyroid.

Therapy: removal or destruction of thyroid

138
Q

What is Hashimoto’s disease?

A

chronic thyroidiyies
loss of capacity to make a thyroid hormones
Hypothyroidism

Antibody and T cells to thyroid. Antigens are generated.

Lymphocyte infiltration Th1 and loss of tissue structure and function.

Therapy: synthetic, thyroid, hormones

139
Q

Causes of disease can be revealed

A

transfer of the condition
Transfer of autoantibodies will cause disease
pregnant, mothers:
Transfer of disease symptoms too baby
only for IgG mediated

140
Q

what is myasthenia gravis

A

organ specific type II like

auto antibodies to ACh receptors on muscle cells
Receptor, uptake and degradation
Muscle is less sensitive to neuronal stimulation

Progressive muscle, weakness:
Droopy, eyelids and double vision
Put the muscles are also affected (chest muscles, leading to raspatory infection)

therapy:
Acetylcholinesterase inhibitors
Immuno suppressants

141
Q

auto antibodies can be…

A

Antagonistic, oh agonistic

142
Q

what is SLE

A

systemic lupus erythematosus
more common in African-Americans and Hispanics

Many auto antibodies lead to too many antigens leads to a wide range of symptoms

malar or butterfly rash is common 50 to 70%

Its affects females, 10 times more than males

20 to 40-year-old s

143
Q

What are the symptoms of SLE?

A

dermatological
Musculoskeletal
Haematological

Inflammation of the lung, liver, kidneys

abs to RBC and platelets
Self destruction by a compliment activation

abs to nuclear antigens are deposited on vascular walls. (immune complex)
information
vasculitis
Activation of compliment and activation of phagocytes

144
Q

how do you diagnose SLE

A

detection against antinuclear antibodies
Directed against:
ss nucleic acid
ds nucleic acid
Nucleoprotein
Histones
nuxleolar RNA

145
Q

what triggers autoimmunity?
Release of sequestered Ag

A

some antigens are Hidden (sequestered)
From the immune system:
Intracellular antigens
Immune privileged sites
T cell tolerance is not establish

Release of hidden, antigens, through trauma or infection, can cause stimulation

146
Q

what is sympathetic ophthalmia

A

trauma to one eye results in the release of hidden intraocular, protein, antigens

released interocular antigen is carried to the lymph nodes and activates T cells

Effector, T cells return via bloodstream, and encounter antigen in both eyes

147
Q

describe in appropriate MHC expression

A

normally a professional antigen presenting cell expresses MHCII

However, in Greaves disease – thyroid axon at cells express MHCII

sensitises T cells to self derived antigens

148
Q

what is molecular mimicry

A

A chance, resemblance of self and a pathogen molecule

This highlights the need for T cells
All autoimmune diseases involve breaking T cell tolerance

149
Q

what is rheumatic feaver

A

follows S.pyogenes infection
Antibodies cross react with a heart, joint and kidneys
Transient autoimmunity as a self antigens don’t stimulate Th cells so antibody production is short lived

150
Q

what is peptide mimicry

A

The same MHC molecule presents both a pathogen peptide and a self peptide that mimics it

Naive, T cell is activated by the pathogen peptide presented by the particular MHC molecule

effector Th1 cell responds to the self peptide, mimic, and activate the macro phage, causing inflammation

Self peptide doesn’t activate the T cell, but once a T cell has been activated by the pathogen peptide…

This lead to chronic information
epitope spreading

151
Q

what is chronic inflammation and epitope spreading?

A

early activation phase:
response to few autoantigens
Autoantigens are never cleared
leading to chronic inflammation

Chronic phase:
Response expand to include more autoantigens
(epitope spreading)

152
Q

what are nucleosomes

A

released from necrotic cells (failed clearance of AC)

a single Th cell stimulated multiple B cells

153
Q

what is the cerebellum and what does it do

A

located at the back/posterior of the brain just above the brain stem and below the occipital lobes

crucial role in co ordinating volountary movements, balance and posture

higher cognitive functions

motor control and conordination

154
Q

where is the temporal lobe and what does it do

A

one if the four main lines in the cerebral cortex. outermost layer of the brain

sides of the brain near the temples

positioned beneath the lateral fissure

auditory processing
language comprehension
memory formation and retrieval
visual processing
emotion and social cognition

155
Q

where is the frontal lobe and what does it do

A

one of the 4 major lives in the cerebral cortex
located at the front of the brain behind the forehead and is speedsters by the parietal lobe and central sulcus

motor control
executive functions
language production
social and emotional processing
higher level cognition

156
Q

Where is it a occipital lobe and what does it do?

A

One of the four main lobes of the cerebral cortex
Located at the posterior region of the brain behind the parietal and temporal lobes.

Visual perception
Visual field mapping
Visual integration
Visual memory

157
Q

where is the central sulcus and what does it do

A

also known as rolandic fissure or central fissure. It is a prominent groove that runs horizontally across the lateral surface of the brain, dividing the frontal lobe from the parietal lobe.

Primary motor cortex
Primary somatosensory cortex
Has a role in the organisation of cortexes

158
Q

where and what does the somatosensory cortex do

A

S1
it is located in the parietal lobe of the brain just behind the central sulcus.

tackles perception tactile perception
proprioception
Plain and temperature perception
Integration with other sensory modalities

159
Q

where is the motor cortex and what does it do

A

primary motor cortex
M1
Located in the frontal lobe of the brain, specifically in the precentral gyrus

primary function of the motor cortex is to control voluntary muscle movements throughout the body

Fine motor control
motor planning
Motor learning
Integration with other brain regions
Initiation and execution of movements